Adiponectin Inhibits the Apoptosis of Cardiomyocytes Induced by Endoplasmic Reticulum Stress After Exposed to Tunicamycin Through p38-MAPK

Aim To investigate the protective effects of adiponectin(APN) on endoplasmic reticulum stress injury of the 3~4 days SD rat cardiomyocytes,which was induced by the tunicamycin and the signaling pathway of its protection.Methods Primary cardiomyocytes were obtained from neonatal rat and cultured by enzymatic digestion methods. The morphology of neonatal rat cardiomyocytes was studied by inverted phase contrast microscope.Its molecular markers were observed by α-actin immunocytochemistry.Primary 3~4 days cells were used in experiment,and they were randomly divided into control group,1 mg/L tunicamycin group(1 mg/L tunicamycin,24 h),1 mg/L tunicamycin+100 mg /L APN group,1 mg/L tunicamycin+3 μmol/L SB203580(the inhibitor of p38-MAPK),1 mg/L tunicamycin+3 μmol/L SB203580+100 mg/L APN group.The change of morphology of cardiomyocytes was observed by inverted phase contrast microscope.The cardiomycocytes apoptosis was detected by Annexin V-FITC / PI flow cytometry.The expressions of GRP78 and CHOP which were molecular markers of endoplasmic reticulum were detected by qRT-PCR and immu-nofluorescence technic.Results Compared with the control group,the apoptosis of cardiomyocytes was significantly increased and the molecular makers of endoplasmic reticulum stress GRP78 and CHOP were greatly increased after exposed to tunicamycin.APN pretreatment significantly decreased the apoptosis rate,and the expression of GRP78 and CHOP.SB203580 pretreatment decreased the protection of APN,the apoptosis was higher compared with 1 mg/L tunicamycin+100 mg/L adponectin group and the expression of GRP78 and CHOP were increased.Compared to 1 mg/L tunicamycin group,the apoptosis was lower and the expression of GRP78 and CHOP was decreased.Conclusion Tunicamycin enhance the expressions of GRP78 and CHOP,and make endoplasmic reticulum stress to start which induces the apoptosis of cardiomyocytes.APN which can attenuate endoplasmic reticulum stress,have a protective effect on myocardial cells.Its protection against endoplasmic reticulum stress was partly through p38-MAPK signaling pathway.