minocycline  (Gold Biotechnology Inc)


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    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/minocycline/product/Gold Biotechnology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    minocycline - by Bioz Stars, 2024-05
    90/100 stars

    Images

    1) Product Images from "Microglia Play an Active Role in Obesity-Associated Cognitive Decline"

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Techniques Used: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Techniques Used: Labeling

    minocycline  (Gold Biotechnology Inc)


    Bioz Verified Symbol Gold Biotechnology Inc is a verified supplier
    Bioz Manufacturer Symbol Gold Biotechnology Inc manufactures this product  
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    Structured Review

    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/minocycline/product/Gold Biotechnology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    minocycline - by Bioz Stars, 2024-05
    90/100 stars

    Images

    1) Product Images from "Microglia Play an Active Role in Obesity-Associated Cognitive Decline"

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Techniques Used: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Techniques Used: Labeling

    minocycline  (Gold Biotechnology Inc)


    Bioz Verified Symbol Gold Biotechnology Inc is a verified supplier
    Bioz Manufacturer Symbol Gold Biotechnology Inc manufactures this product  
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    Structured Review

    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/minocycline/product/Gold Biotechnology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    minocycline - by Bioz Stars, 2024-05
    90/100 stars

    Images

    1) Product Images from "Microglia Play an Active Role in Obesity-Associated Cognitive Decline"

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Techniques Used: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Techniques Used: Labeling

    minocycline  (Gold Biotechnology Inc)


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    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Microglia Play an Active Role in Obesity-Associated Cognitive Decline"

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Techniques Used: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Techniques Used: Labeling

    minocycline  (Gold Biotechnology Inc)


    Bioz Verified Symbol Gold Biotechnology Inc is a verified supplier
    Bioz Manufacturer Symbol Gold Biotechnology Inc manufactures this product  
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    Structured Review

    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/minocycline/product/Gold Biotechnology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    minocycline - by Bioz Stars, 2024-05
    90/100 stars

    Images

    1) Product Images from "Microglia Play an Active Role in Obesity-Associated Cognitive Decline"

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Techniques Used: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.
    Figure Legend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Techniques Used: Labeling

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    Gold Biotechnology Inc minocycline
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Gold Biotechnology Inc minocycline
    <t>Minocycline</t> treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).
    Minocycline, supplied by Gold Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/minocycline/product/Gold Biotechnology Inc
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    minocycline - by Bioz Stars, 2024-05
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    Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Journal: The Journal of Neuroscience

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Figure Lengend Snippet: Minocycline treatment prevents obesity-associated microglial activation and cognitive decline. A, Weekly body weight measurements for mice fed HFD for 12 weeks showed characteristic weight gain with no differences with minocycline treatment (n = 20 for each group, week: F(12,456) = 262.2, p < 0.0001; treatment group: F(1,38) = 0.051, p = 0.82; and week × treatment: F(12,456) = 0.64, p = 0.81, two-way ANOVA). Bracket indicates the duration of minocycline treatment. The MOL of the DG (B) and the RAD (C) of the CA1 region immunolabeled with iba1 (green) and CD68 (red). Scale bar, 10 μm. Arrows indicate CD68 and iba1 colabeling. D, Microglial mean activation scores in the MOL (t(18) = 2.60, p = 0.018, unpaired t test) and RAD (t(18) = 2.84, p = 0.011, unpaired t test) of the hippocampus were reduced with minocycline treatment. N = 10 for each group (10 cells were averaged per animal). E, Obesity-induced impairments in DRs in the OL test were improved by minocycline treatment in obese mice (diet group: F(1,38) = 6.38, p = 0.016; treatment group: F(1,38) = 1.94, p = 0.17; and diet × treatment: F(1,38) = 5.38, p = 0.026, two-way ANOVA). Holm–Sidak post hoc comparisons show a lower DR in obese + vehicle compared with control + vehicle (t(38) = 3.43, p = 0.009), control + minocycline (t(38) = 2.77, p = 0.042), and obese + minocycline (t(38) = 2.69, p = 0.042). F, While time spent exploring the objects during the test phase of OL was altered by minocycline treatment (diet group: F(1,38) = 0.75, p = 0.39; treatment group: F(1,38) = 4.21, p = 0.047; and diet × treatment: F(1,38) = 0.84, p = 0.36, two-way ANOVA), Holm–Sidak post hoc comparisons did not reveal any differences between groups. E, F, n = 10 for control + vehicle and control + minocycline, and n = 11 for obese + vehicle and obese + minocycline. Error bars indicate SEM. *p < 0.05 compared with untreated obese mice (D) or compared with all other groups (E).

    Article Snippet: After ∼10 weeks of HFD exposure, mice were given access to either water or water treated with minocycline (40 mg/kg per mouse; Gold Biotechnology).

    Techniques: Activation Assay, Immunolabeling

    Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Journal: The Journal of Neuroscience

    Article Title: Microglia Play an Active Role in Obesity-Associated Cognitive Decline

    doi: 10.1523/JNEUROSCI.0789-18.2018

    Figure Lengend Snippet: Minocycline treatment prevents obesity-associated dendritic spine loss. Images of dendritic segments labeled with DiI on dendrites of DG GCs (A) and on apical dendrites (B) of CA1 pyramidal cells from control and obese mice treated with minocycline. Scale bar, 5 μm. Arrows indicate dendritic spines. C, Obesity-induced decreases in dendritic spine density on GC dendrites of the DG were increased in minocycline-treated obese mice (diet group: F(1,19) = 5.01, p = 0.037; treatment group: F(1,19) = 4.91, p = 0.039; and diet × treatment: F(1,19) = 3.56, p = 0.075, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(19) = 2.97, p = 0.031), control + minocycline (t(19) = 3.20, p = 0.028), and obese + minocycline (t(19) = 3.11, p = 0.029). D, Obesity-induced decreases in dendritic spine density on apical dendrites of CA1 pyramidal cells were increased in minocycline-treated obese mice (diet group: F(1,18) = 14.67, p = 0.0012; treatment group: F(1,18) = 3.87, p = 0.065; and diet × treatment: F(1,18) = 3.42, p = 0.081, two-way ANOVA). Holm–Sidak post hoc comparisons show lower dendritic spine numbers in obese + vehicle compared with control + vehicle (t(18) = 4.02, p = 0.0041), control + minocycline (t(18) = 4.10, p = 0.0040), and obese + minocycline (t(18) = 2.83, p = 0.044). n = 5 for control + vehicle and control + minocycline, n = 7 for obese + vehicle (D; n = 6 for obese + vehicle), and n = 6 for obese + minocycline (50 spines analyzed per animal). Error bars indicate SEM. *p < 0.05 compared with all other groups.

    Article Snippet: After ∼10 weeks of HFD exposure, mice were given access to either water or water treated with minocycline (40 mg/kg per mouse; Gold Biotechnology).

    Techniques: Labeling