SB 202190 was used to inhibit p38 activation in MCF7 cells5, mouse macrophages6 and HepG2 cells.7
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1) Product Images from "CTRP9 Mediates Protective Effects in Cardiomyocytes via AMPK- and Adiponectin Receptor-Mediated Induction of Anti-Oxidant Response"
Article Title: CTRP9 Mediates Protective Effects in Cardiomyocytes via AMPK- and Adiponectin Receptor-Mediated Induction of Anti-Oxidant Response
Figure Legend Snippet: Signaling pathways involved in CTRP9 effects in cardiomyocytes and cardiomyoblasts. ( A ) Densitometry and representative Western blots, showing the time-dependent influence of CTRP9 (4 µg/mL) on the activation of AMPK, p44/42 MAPK, p38 MAPK and Akt in ARVCs. n = cells from 13–14 different animals per group. ( B ) Influence of AMPK inhibition with Ara A (500 µmol/L), p44/42 MAPK inhibition with U0126 (10 µmol/L) or p38 MAPK inhibition with SB 202190 (5 µmol/L) on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in ARVCs in response to phenylephrine (10 µmol/L). Inhibitors were applied 30 min before CTRP9 (4 µg/mL, 24 h). n = cells from five different animals per group. ( C ): Mitochondrial and cytosolic ROS release in H9C2 cardiomyoblasts after alpha1 or alpha2-AMPK knockdown by siRNA. Mock transfected cells served as controls. 24 h after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (protein) is shown. Data from 5 independent experiments. ( D ) Influence of exclusive knockdown of AdipoR1, AdipoR2, or T-cadherin on CTRP9-mediated anti-oxidative effects as deduced from changes of DCFH-DA fluorescence in H9C2 cardiomyoblasts. Twenty-four hours after transfection, cells were pre-incubated with CTRP9 (4 µg/mL) for 24 h and then treated with phenylephrine. Knockdown efficiency (mRNA) is shown. Data from five independent experiments. ( E ) Influence of combined knockdown of AdipoR1 and AdipoR2 on CTRP9-mediated anti-oxidative effects as described in D. Data from five independent experiments. ( F ) Influence of knockdown of calreticulin or gC1qR on CTRP9-mediated anti-oxidative effects as described in D. Knockdown efficiency (protein) is shown. Data from five independent experiments. All data are mean ± SEM, * p
Techniques Used: Western Blot, Activation Assay, Inhibition, Acetylene Reduction Assay, Fluorescence, Transfection, Incubation
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Article Snippet: Reagents Phorbol 12-myristate 13-acetate (PMA), the calcium ionophore ionomycin, FK506, and the protein kinase inhibitors H89, LY294002, PD98059, SB202190, SB203580, SP600125 and