dmso  (Alomone Labs)


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    Structured Review

    Alomone Labs dmso
    TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist <t>A967079</t> (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % <t>DMSO,</t> 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p
    Dmso, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dmso/product/Alomone Labs
    Average 94 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    dmso - by Bioz Stars, 2022-08
    94/100 stars

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    1) Product Images from "Dysfunctional TRPM8 signalling in the vascular response to environmental cold in ageing"

    Article Title: Dysfunctional TRPM8 signalling in the vascular response to environmental cold in ageing

    Journal: eLife

    doi: 10.7554/eLife.70153

    TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist A967079 (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % DMSO, 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p
    Figure Legend Snippet: TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist A967079 (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % DMSO, 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p

    Techniques Used: Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot

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    Alomone Labs bq 788
    Systemic administration of an ET A receptor antagonist, but not an ET B receptor antagonist, prevented oxaliplatin-induced mechanical allodynia and cold allodynia: Mechanical allodynia (a, b, d) and cold allodynia (c, e) were examined using the von Frey test and the acetone test, respectively. An ET A receptor antagonist, atrasentan (a–c), or an ET B receptor antagonist, <t>BQ-788</t> (d, e), was intraperitoneally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–8). (a, d) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (c, e) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h, 24 h and 4 days after oxaliplatin administration. * p
    Bq 788, supplied by Alomone Labs, 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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    92
    Alomone Labs fasciculin ii
    Generation of muscle-specific Arhgef5 KO mice. (A) Strategy for the generation of conditional Arhgef5 knockouts. Mice with loxP sites flanking the third exon of Arhgef5 were crossed with Cre-recombinase expressing mice to produce knockout. (B) Genotyping shows successful recombination in the muscles but not tail tipss of AG5 fl/fl ; Acta-Cre mice. (C) Quantification of Arhgef5 mRNA expression in AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice at 50 and 500 days of age. Results are mean ± SEM of three mice from each genotype. (D) Proper alignment of pre- and post-synaptic elements in AG5 fl/fl ; Acta-Cre muscles. Single fibers of tibialis anterior muscles isolated from AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice were stained with BTX (to visualize AChR), <t>fasciculin</t> II (to visualize the synaptic cleft marker acetylcholinesterase), and anti-neurofilament + anti-synaptophysin antibodies (to visualize the presynaptic nerve terminal). Scale bar is 20 μm. ∗ p
    Fasciculin Ii, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs l689 560
    a) Bath application of <t>L689</t> during stimulation induces activity-dependent depotentiation of dorsal horn LTP in spinal cord explants from female C57BL/6 mice. b) Antagonism at the NMDA receptor glutamate-binding site via APV does not reverse dorsal horn LTP, but instead further potentiates fPSPs after drug administration. 7-CK with stimulation: n = 14, t (13) = 3.514, ** p = 0.0038; L689 with stimulation: n = 7, t (6) = 2.845, * p = 0.0294; APV with stimulation: n = 7, t (6) = 4.033, ** p = 0.0069.
    L689 560, supplied by Alomone Labs, 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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    94
    Alomone Labs dmso
    TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist <t>A967079</t> (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % <t>DMSO,</t> 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p
    Dmso, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dmso/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dmso - by Bioz Stars, 2022-08
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    Image Search Results


    Systemic administration of an ET A receptor antagonist, but not an ET B receptor antagonist, prevented oxaliplatin-induced mechanical allodynia and cold allodynia: Mechanical allodynia (a, b, d) and cold allodynia (c, e) were examined using the von Frey test and the acetone test, respectively. An ET A receptor antagonist, atrasentan (a–c), or an ET B receptor antagonist, BQ-788 (d, e), was intraperitoneally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–8). (a, d) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (c, e) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h, 24 h and 4 days after oxaliplatin administration. * p

    Journal: Molecular Pain

    Article Title: Endothelin receptor type A is involved in the development of oxaliplatin-induced mechanical allodynia and cold allodynia acting through spinal and peripheral mechanisms in rats

    doi: 10.1177/17448069211058004

    Figure Lengend Snippet: Systemic administration of an ET A receptor antagonist, but not an ET B receptor antagonist, prevented oxaliplatin-induced mechanical allodynia and cold allodynia: Mechanical allodynia (a, b, d) and cold allodynia (c, e) were examined using the von Frey test and the acetone test, respectively. An ET A receptor antagonist, atrasentan (a–c), or an ET B receptor antagonist, BQ-788 (d, e), was intraperitoneally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–8). (a, d) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (c, e) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h, 24 h and 4 days after oxaliplatin administration. * p

    Article Snippet: Oxaliplatin (Yakult Corporation, Tokyo, Japan) was diluted in 5% glucose solution (1 mg/mL) and intraperitoneally administered at a dose of 5 mg/kg at day 0. , Bosentan, a dual ETA /ETB receptor antagonist (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), atrasentan, a selective ETA receptor antagonist (Sigma-Aldrich, St Louis, MO, USA) and BQ-788, a selective ETB receptor antagonist (Alomone Labs, Jerusalem, Israel) were dissolved in 60% dimethylsulfoxide and 40% propylene glycol.

    Techniques:

    Intrathecal administration of an ET A receptor antagonist prevented oxaliplatin-induced mechanical allodynia but not cold allodynia: Mechanical allodynia (a, c) and cold allodynia (b, d) were examined using the von Frey test and the acetone test, respectively. Atrasentan (50 μg) or BQ-788 (50 μg) was intrathecally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–6). (a, c) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (b, d) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h and 24 h after oxaliplatin administration. * p

    Journal: Molecular Pain

    Article Title: Endothelin receptor type A is involved in the development of oxaliplatin-induced mechanical allodynia and cold allodynia acting through spinal and peripheral mechanisms in rats

    doi: 10.1177/17448069211058004

    Figure Lengend Snippet: Intrathecal administration of an ET A receptor antagonist prevented oxaliplatin-induced mechanical allodynia but not cold allodynia: Mechanical allodynia (a, c) and cold allodynia (b, d) were examined using the von Frey test and the acetone test, respectively. Atrasentan (50 μg) or BQ-788 (50 μg) was intrathecally administered for 2 consecutive days (days −1 and 0) before intraperitoneal oxaliplatin administration (5 mg/kg) on day 0 ( n = 5–6). (a, c) Mechanical allodynia was examined before each drug administration and 2 h, 8 h, 24 h, 4 days, 7 days, 11 days, 14 days, 21 days, and 28 days after oxaliplatin administration. (b, d) Cold allodynia was examined before atrasentan, BQ-788 and oxaliplatin administration and 2 h, 8 h and 24 h after oxaliplatin administration. * p

    Article Snippet: Oxaliplatin (Yakult Corporation, Tokyo, Japan) was diluted in 5% glucose solution (1 mg/mL) and intraperitoneally administered at a dose of 5 mg/kg at day 0. , Bosentan, a dual ETA /ETB receptor antagonist (Tokyo Chemical Industry Co., Ltd., Tokyo, Japan), atrasentan, a selective ETA receptor antagonist (Sigma-Aldrich, St Louis, MO, USA) and BQ-788, a selective ETB receptor antagonist (Alomone Labs, Jerusalem, Israel) were dissolved in 60% dimethylsulfoxide and 40% propylene glycol.

    Techniques:

    Generation of muscle-specific Arhgef5 KO mice. (A) Strategy for the generation of conditional Arhgef5 knockouts. Mice with loxP sites flanking the third exon of Arhgef5 were crossed with Cre-recombinase expressing mice to produce knockout. (B) Genotyping shows successful recombination in the muscles but not tail tipss of AG5 fl/fl ; Acta-Cre mice. (C) Quantification of Arhgef5 mRNA expression in AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice at 50 and 500 days of age. Results are mean ± SEM of three mice from each genotype. (D) Proper alignment of pre- and post-synaptic elements in AG5 fl/fl ; Acta-Cre muscles. Single fibers of tibialis anterior muscles isolated from AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice were stained with BTX (to visualize AChR), fasciculin II (to visualize the synaptic cleft marker acetylcholinesterase), and anti-neurofilament + anti-synaptophysin antibodies (to visualize the presynaptic nerve terminal). Scale bar is 20 μm. ∗ p

    Journal: Frontiers in Molecular Neuroscience

    Article Title: Arhgef5 Binds α-Dystrobrevin 1 and Regulates Neuromuscular Junction Integrity

    doi: 10.3389/fnmol.2020.00104

    Figure Lengend Snippet: Generation of muscle-specific Arhgef5 KO mice. (A) Strategy for the generation of conditional Arhgef5 knockouts. Mice with loxP sites flanking the third exon of Arhgef5 were crossed with Cre-recombinase expressing mice to produce knockout. (B) Genotyping shows successful recombination in the muscles but not tail tipss of AG5 fl/fl ; Acta-Cre mice. (C) Quantification of Arhgef5 mRNA expression in AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice at 50 and 500 days of age. Results are mean ± SEM of three mice from each genotype. (D) Proper alignment of pre- and post-synaptic elements in AG5 fl/fl ; Acta-Cre muscles. Single fibers of tibialis anterior muscles isolated from AG5 fl/fl and AG5 fl/fl ; Acta-Cre mice were stained with BTX (to visualize AChR), fasciculin II (to visualize the synaptic cleft marker acetylcholinesterase), and anti-neurofilament + anti-synaptophysin antibodies (to visualize the presynaptic nerve terminal). Scale bar is 20 μm. ∗ p

    Article Snippet: For visualization of AChR we used fluorescently labeled α-bungarotoxin (B35451 or B13422; Thermo), and for visualizing the synaptic cleft, we used fasciculin II, which binds to acetylcholinesterase (F-225; Alomone Labs, labeled with FluoReporter FITC kit from Thermo).

    Techniques: Mouse Assay, Expressing, Knock-Out, Isolation, Staining, Marker

    a) Bath application of L689 during stimulation induces activity-dependent depotentiation of dorsal horn LTP in spinal cord explants from female C57BL/6 mice. b) Antagonism at the NMDA receptor glutamate-binding site via APV does not reverse dorsal horn LTP, but instead further potentiates fPSPs after drug administration. 7-CK with stimulation: n = 14, t (13) = 3.514, ** p = 0.0038; L689 with stimulation: n = 7, t (6) = 2.845, * p = 0.0294; APV with stimulation: n = 7, t (6) = 4.033, ** p = 0.0069.

    Journal: bioRxiv

    Article Title: Spinal reconsolidation engages non-ionotropic NMDA receptor signaling to reverse pain hypersensitivity

    doi: 10.1101/2021.09.08.458120

    Figure Lengend Snippet: a) Bath application of L689 during stimulation induces activity-dependent depotentiation of dorsal horn LTP in spinal cord explants from female C57BL/6 mice. b) Antagonism at the NMDA receptor glutamate-binding site via APV does not reverse dorsal horn LTP, but instead further potentiates fPSPs after drug administration. 7-CK with stimulation: n = 14, t (13) = 3.514, ** p = 0.0038; L689 with stimulation: n = 7, t (6) = 2.845, * p = 0.0294; APV with stimulation: n = 7, t (6) = 4.033, ** p = 0.0069.

    Article Snippet: L689-560 was obtained from Alomone Labs (Jerusalem, Israel).

    Techniques: Activity Assay, Mouse Assay, Binding Assay

    TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist A967079 (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % DMSO, 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p

    Journal: eLife

    Article Title: Dysfunctional TRPM8 signalling in the vascular response to environmental cold in ageing

    doi: 10.7554/eLife.70153

    Figure Lengend Snippet: TRPA1 and TRPM8 are involved in cold-induced vascular response. Vascular responses with cold (4 °C) water treatment in mice pre-treated with combined TRPA1 antagonist A967079 (100 mg kg –1 ) and TRPM8 antagonist AMTB (10 mg kg –1 ), or vehicle control (Veh - 10 % DMSO, 10 % Tween in saline) i.p. 30 min before cold treatment. ( a–c ) % change in hindpaw blood flow from baseline to 0–2 min following cold treatment (maximum vasoconstriction) in mice treated with combined antagonist ( a ) A967079+ AMTB, ( b ) A967079, and ( c ) AMTB. ( d-f ) Maximum vasoconstriction caused by cold water treatment in mice treated with combined antagonist ( d ) A967079+ AMTB, ( e ) A967079, and ( f ) AMTB normalised against vehicle treated mice. (n = 5–10) ( g–h ) RT-PCR CT analysis shows fold change of ( g ) Trpa1 and ( h ) Trpm8 normalised to three housekeeping genes in DRG. (n = 14–15) ( i ) Representative western blot of TRPM8 in DRG of young and aged mice and densitometric analysis normalised to Tubulin (Y = young, A = aged) (n = 9). All results are shown as mean ± s.e.m. *p

    Article Snippet: The TRPA1 antagonist A967079 ((1E,3E)–1-(4-Fluorophenyl)–2-methyl-1-pentene-3-one oxime); (Alomone Labs, # A-225) was dissolved in 10 % DMSO (Dimethyl sulfoxide) with 10 % Tween-80 in saline.

    Techniques: Mouse Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot