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skatole  (MedChemExpress)


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    MedChemExpress skatole
    Skatole, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/skatole/product/MedChemExpress
    Average 93 stars, based on 10 article reviews
    skatole - by Bioz Stars, 2026-02
    93/100 stars

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    MedChemExpress hy w007355
    Irisin inhibited calcium overload, ER stress and remodeling in VSMCs and aortic tissues with Ang II exposure via αV/β5 receptor-AMPK/p38 pathway. A and B. The effect of irisin supplementation on the expression levels of ERS-related proteins and kinases (AMPK and p38) in Ang II-treated VSMCs was evaluated by immunoblotting. VSMCs were treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). C. Intracellular calcium levels in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). D-E. The levels of phosphorylated- and total-AMPK and p38 in lysates of aortic tissues from WT, irisin-KO, and irisin-OV mice infused with saline or Ang II (490 ng/min/kg) for 4 weeks were detected using immunoblotting (n=3/group). F. Edu incorporation assay evaluated the proliferation ability of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or <t>HY-W007355</t> (a p38 activator, 10 μM) for 24 h (n=4/group). G. Transwell migration assay evaluated the migration of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). H. Phenotypic switching indicated by the mRNA expressions of VSMC-specific contractile genes (including SMA, SM22, calponin, and caldesmon1) in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). The data were presented as mean ± S.E.M., and the statistical analyses were performed by one way ANOVA. *P < 0.05 and **P < 0.01. Ctrl, control; I, irisin; Ang II, angiotensin II; SMA, SM α-actin; SM22, smooth muscle 22 alpha; WT, wild type mice; KO, irisin knockout mice; OV, irisin overexpression mice.
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    Irisin inhibited calcium overload, ER stress and remodeling in VSMCs and aortic tissues with Ang II exposure via αV/β5 receptor-AMPK/p38 pathway. A and B. The effect of irisin supplementation on the expression levels of ERS-related proteins and kinases (AMPK and p38) in Ang II-treated VSMCs was evaluated by immunoblotting. VSMCs were treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). C. Intracellular calcium levels in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). D-E. The levels of phosphorylated- and total-AMPK and p38 in lysates of aortic tissues from WT, irisin-KO, and irisin-OV mice infused with saline or Ang II (490 ng/min/kg) for 4 weeks were detected using immunoblotting (n=3/group). F. Edu incorporation assay evaluated the proliferation ability of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). G. Transwell migration assay evaluated the migration of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). H. Phenotypic switching indicated by the mRNA expressions of VSMC-specific contractile genes (including SMA, SM22, calponin, and caldesmon1) in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). The data were presented as mean ± S.E.M., and the statistical analyses were performed by one way ANOVA. *P < 0.05 and **P < 0.01. Ctrl, control; I, irisin; Ang II, angiotensin II; SMA, SM α-actin; SM22, smooth muscle 22 alpha; WT, wild type mice; KO, irisin knockout mice; OV, irisin overexpression mice.

    Journal: International Journal of Biological Sciences

    Article Title: Irisin attenuates vascular remodeling in hypertensive mice induced by Ang II by suppressing Ca 2+ -dependent endoplasmic reticulum stress in VSMCs

    doi: 10.7150/ijbs.84153

    Figure Lengend Snippet: Irisin inhibited calcium overload, ER stress and remodeling in VSMCs and aortic tissues with Ang II exposure via αV/β5 receptor-AMPK/p38 pathway. A and B. The effect of irisin supplementation on the expression levels of ERS-related proteins and kinases (AMPK and p38) in Ang II-treated VSMCs was evaluated by immunoblotting. VSMCs were treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). C. Intracellular calcium levels in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody (n=3/group). D-E. The levels of phosphorylated- and total-AMPK and p38 in lysates of aortic tissues from WT, irisin-KO, and irisin-OV mice infused with saline or Ang II (490 ng/min/kg) for 4 weeks were detected using immunoblotting (n=3/group). F. Edu incorporation assay evaluated the proliferation ability of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). G. Transwell migration assay evaluated the migration of VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). H. Phenotypic switching indicated by the mRNA expressions of VSMC-specific contractile genes (including SMA, SM22, calponin, and caldesmon1) in VSMCs treated with irisin (20 nM) or Ang II (1 μM) alone, or irisin (20 nM) in combination with Ang II (1 μM) in the absence and presence of αV/β5 antibody, or compound C (an AMPK inhibitor, 5 μM), or HY-W007355 (a p38 activator, 10 μM) for 24 h (n=4/group). The data were presented as mean ± S.E.M., and the statistical analyses were performed by one way ANOVA. *P < 0.05 and **P < 0.01. Ctrl, control; I, irisin; Ang II, angiotensin II; SMA, SM α-actin; SM22, smooth muscle 22 alpha; WT, wild type mice; KO, irisin knockout mice; OV, irisin overexpression mice.

    Article Snippet: Compound C and HY-W007355 were purchased from MedChemExpress (NJ, USA).

    Techniques: Expressing, Western Blot, Saline, Transwell Migration Assay, Migration, Control, Knock-Out, Over Expression