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Proanthocyanidin protects H9C2 cells against hypoxia/reoxygenation injury via JAK2/STAT3 signaling pathway
Pages: 568-574
Year: Issue:  5
Journal: Acta Physiologica Sinica

Keyword:  proanthocyanidinhypoxia/reoxygenation injuryJAK2/STAT3oxidative stressendoplasmic reticulum stress;
Abstract: The present study was aimed to investigate the underlying mechanisms of the protective effect of proanthocyanidin(Pro) against hypoxia/reoxygenation(H/R) injury in H9C2 cells with a focus on Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) signaling pathway. H9C2 cells were randomly assigned to 5 groups, including the control group(Con), the H/R-injured group(H/R), the Pro-treated group(H/R+Pro), the JAK2 si RNA-treated group(H/R+Pro+JAK2 si RNA) and the JAK2 si RNA control group(H/R+JAK2 si RNA). The cells were pretreated with Pro(40 μmol/L) for 8 h before 2 h of hypoxia and 4 h of reoxygenation. Cellular viability and apoptosis rate were detected by MTT and TUNEL methods, and superoxide generation was measured. JAK2/STAT3 signaling, oxidative stress markers and endoplasmic reticulum stress markers were also detected by Western blot. We found that Pro treatment significantly improved cellular viability and reduced apoptosis rate in H/R-treated H9C2 cells. In addition, Pro treatment significantly up-regulated the phosphorylation levels of JAK2 and STAT3, down-regulated the superoxide generation, gp91phox, glucose-regulated protein 78(GRP78), CCAAT/enhancer binding protein homologous protein(CHOP) and caspase-12 expression. However, these protective effects of Pro were all attenuated by JAK2 si RNA administration. Taken together, we demonstrated that Pro protects H9C2 cells against H/R-induced oxidative stress and endoplasmic reticulum stress injury via JAK2/STAT3 signaling pathway.
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