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    MedChemExpress ne 100
    Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , <t>NE-100,</t> and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p
    Ne 100, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Stimulation of Sigma-1 Receptor Protects against Cardiac Fibrosis by Alleviating IRE1 Pathway and Autophagy Impairment"

    Article Title: Stimulation of Sigma-1 Receptor Protects against Cardiac Fibrosis by Alleviating IRE1 Pathway and Autophagy Impairment

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/8836818

    Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , NE-100, and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p
    Figure Legend Snippet: Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , NE-100, and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p

    Techniques Used: Inhibition, Activation Assay, Western Blot, Immunofluorescence, Staining, EdU Assay, Wound Healing Assay

    Sig1R protects against cardiac fibrosis by attenuating autophagic flux impairment. (a, b) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of LC3 and p62 in mice heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, h) The mRFP-GFP-LC3 expressing cells were visualized by confocal microscopy. Merged fluorescence from RFP and GFP was assessed with Pearson's correlation coefficient, and 20 cells were used for quantification in each group. Scale bar = 5 μ m. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p
    Figure Legend Snippet: Sig1R protects against cardiac fibrosis by attenuating autophagic flux impairment. (a, b) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of LC3 and p62 in mice heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, h) The mRFP-GFP-LC3 expressing cells were visualized by confocal microscopy. Merged fluorescence from RFP and GFP was assessed with Pearson's correlation coefficient, and 20 cells were used for quantification in each group. Scale bar = 5 μ m. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Techniques Used: Western Blot, Mouse Assay, Injection, Expressing, Confocal Microscopy, Fluorescence

    Sig1R protects against cardiac fibrosis by inhibition of ER stress. (a, b) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, i) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, thapsigargin treatment only (Th), fluvoxamine treatment, and thapsigargin combined fluvoxamine treatment (Th+FLV) groups. n = 3; (h, j) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, 4-PBA treatment only (4-PBA), NE-100 treatment (NE-100), and NE-100 combined 4-PBA treatment (N+4-PBA) groups. (k, l) The protein levels of POSTN and CTGF in cardiac fibroblasts from different groups. n = 3. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p
    Figure Legend Snippet: Sig1R protects against cardiac fibrosis by inhibition of ER stress. (a, b) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, i) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, thapsigargin treatment only (Th), fluvoxamine treatment, and thapsigargin combined fluvoxamine treatment (Th+FLV) groups. n = 3; (h, j) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, 4-PBA treatment only (4-PBA), NE-100 treatment (NE-100), and NE-100 combined 4-PBA treatment (N+4-PBA) groups. (k, l) The protein levels of POSTN and CTGF in cardiac fibroblasts from different groups. n = 3. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Techniques Used: Inhibition, Western Blot, Injection

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    MedChemExpress ne 100
    Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , <t>NE-100,</t> and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p
    Ne 100, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ne 100/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
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    Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , NE-100, and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Stimulation of Sigma-1 Receptor Protects against Cardiac Fibrosis by Alleviating IRE1 Pathway and Autophagy Impairment

    doi: 10.1155/2021/8836818

    Figure Lengend Snippet: Inhibition of Sig1R further promotes cardiac fibroblast activation. Cardiac fibroblasts were randomly divided into four groups: control, TGF- β , NE-100, and NE-100+TGF- β 1. (a, b) The representative western blot results of POSTN, CTGF, and TGF- β in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (c) Representative of immunofluorescence staining showed α -SMA (green) in cardiac fibroblasts from different groups. Scale bar = 20 μ m, n = 100 (d, f) The proliferation rate of cardiac fibroblasts from different groups was assessed by EdU assay. Scale bar = 100 μ m, n = 200; (e, g) Scratch wound-healing assay in cardiac fibroblasts from different groups; images were taken at 0 and 24 h postscratch. Black lines denote the wound borders. Scale bar = 100 μ m. n = 6. Shown are representative pictures, p was determined by one-way ANOVA analysis. ∗ p

    Article Snippet: The following reagents were used: TGF- β 1 (10 ng/ml, Sino Biology), fluvoxamine (MCE, HY-B0103A), NE-100 (Sigma-Aldrich, SML0631), 4μ8C (MCE, HY-19707), thapsigargin (MCE, HY-13433), and 4-PBA (Sigma-Aldrich, SML0309).

    Techniques: Inhibition, Activation Assay, Western Blot, Immunofluorescence, Staining, EdU Assay, Wound Healing Assay

    Sig1R protects against cardiac fibrosis by attenuating autophagic flux impairment. (a, b) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of LC3 and p62 in mice heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, h) The mRFP-GFP-LC3 expressing cells were visualized by confocal microscopy. Merged fluorescence from RFP and GFP was assessed with Pearson's correlation coefficient, and 20 cells were used for quantification in each group. Scale bar = 5 μ m. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Stimulation of Sigma-1 Receptor Protects against Cardiac Fibrosis by Alleviating IRE1 Pathway and Autophagy Impairment

    doi: 10.1155/2021/8836818

    Figure Lengend Snippet: Sig1R protects against cardiac fibrosis by attenuating autophagic flux impairment. (a, b) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of LC3 and p62 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of LC3 and p62 in mice heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, h) The mRFP-GFP-LC3 expressing cells were visualized by confocal microscopy. Merged fluorescence from RFP and GFP was assessed with Pearson's correlation coefficient, and 20 cells were used for quantification in each group. Scale bar = 5 μ m. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Article Snippet: The following reagents were used: TGF- β 1 (10 ng/ml, Sino Biology), fluvoxamine (MCE, HY-B0103A), NE-100 (Sigma-Aldrich, SML0631), 4μ8C (MCE, HY-19707), thapsigargin (MCE, HY-13433), and 4-PBA (Sigma-Aldrich, SML0309).

    Techniques: Western Blot, Mouse Assay, Injection, Expressing, Confocal Microscopy, Fluorescence

    Sig1R protects against cardiac fibrosis by inhibition of ER stress. (a, b) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, i) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, thapsigargin treatment only (Th), fluvoxamine treatment, and thapsigargin combined fluvoxamine treatment (Th+FLV) groups. n = 3; (h, j) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, 4-PBA treatment only (4-PBA), NE-100 treatment (NE-100), and NE-100 combined 4-PBA treatment (N+4-PBA) groups. (k, l) The protein levels of POSTN and CTGF in cardiac fibroblasts from different groups. n = 3. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Stimulation of Sigma-1 Receptor Protects against Cardiac Fibrosis by Alleviating IRE1 Pathway and Autophagy Impairment

    doi: 10.1155/2021/8836818

    Figure Lengend Snippet: Sig1R protects against cardiac fibrosis by inhibition of ER stress. (a, b) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, fluvoxamine treatment (FLV), or fluvoxamine combined with TGF- β 1 treatment (FLV+TGF- β ) groups. n = 3; (c, d) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in cardiac fibroblasts from control, TGF- β 1 treatment (TGF- β ) groups, NE-100 treatment (NE-100), or NE-100 combined with TGF- β 1 treatment (N+TGF- β ) groups. n = 3; (e, f) The representative western blot results of p-PERK, p-IRE1 α , ATF4, XBP1s, and c-ATF6 in heart tissue from sham-operated (Sham), TAC, and intraperitoneal injection with fluvoxamine after TAC (FLV) groups. n = 6; (g, i) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, thapsigargin treatment only (Th), fluvoxamine treatment, and thapsigargin combined fluvoxamine treatment (Th+FLV) groups. n = 3; (h, j) The representative western blot results of POSTN and CTGF in cardiac fibroblasts from control, 4-PBA treatment only (4-PBA), NE-100 treatment (NE-100), and NE-100 combined 4-PBA treatment (N+4-PBA) groups. (k, l) The protein levels of POSTN and CTGF in cardiac fibroblasts from different groups. n = 3. Shown are representative pictures, p value was determined by one-way ANOVA with Tukey post hoc analysis. ∗ p

    Article Snippet: The following reagents were used: TGF- β 1 (10 ng/ml, Sino Biology), fluvoxamine (MCE, HY-B0103A), NE-100 (Sigma-Aldrich, SML0631), 4μ8C (MCE, HY-19707), thapsigargin (MCE, HY-13433), and 4-PBA (Sigma-Aldrich, SML0309).

    Techniques: Inhibition, Western Blot, Injection