Effect of Diosgenin on Coxsackievirusinduced Cardiomyocyte Injury via Inhibition of Endoplasmic Reticulum Stress
Coxsackievirus B3(CVB3)is the most common pathogenic strain of viral myocarditis.The effect of CVB3 infection on cardiomyocyte injury is related to activation of endoplasmic reticulum stress(ERS).Diosgenin alleviates hypoxic injury to cardiomyocytes by inhibiting ERS.However,the protective effect of diosgenin on CVB3 infectioninduced cardiomyocyte injury and its mechanism of action are not known.We analyzed the effect and mechanism of action of diosgenin on CVB3induced cardiomyocyte injury by inhibiting ERS.Myocardial(H9c2)cells were cultured and divided into groups.The control group was treated with medium free of drugs or viruses.The model group was treated with medium containing CVB3 and diosgenin(10,20,40 mg/L).The solvent control group was treated with medium containing the control solvent dimethyl sulfoxide(DMSO).The solvent+model group was treated with medium containing DMSO and CVB3.The solvent+diosgenin group was treated with medium containing DMSO,CVB3 and diosgenin(40 mg/L).The agonist+diosgenin group was treated with medium containing an ERS agonist,CVB3 and diosgenin(40 mg/L).The content of lactate dehydrogenase(LDH),creatine kinase(CK),and creatine kinase isoenzymeMB(CKMB)in the medium,viability of A490 cells,and apoptosis rate,as well as expression of the ERS marker glucoseregulated protein 78(GRP78),C/EBP homologous protein(CHOP),phosphorylated CJun aminoterminal kinase(pJNK),and cleaved caspase12 in cells were determined.Compared with the control group,the content of LDH,CK,and CKMB in the medium,apoptosis rate,and expression of GRP78,CHOP,pJNK,and cleaved caspase12 in cells of the model group increased,while the viability of A490 cells decreased.Compared with the model group,the content of LDH,CK,and CKMB in the medium,apoptosis rate,and expression of GRP78,CHOP,pJNK,and cleaved caspase12 in cells of the model group decreased,while the viability of A490 cells increased.Compared with the solvent+diosgenin group,the content of LDH,CK,and CKMB in the medium,apoptosis rate,and expression of GRP78,CHOP,pJNK,and cleaved caspase12 in cells of the model group increased,while the viability of A490 cells decreased in the agonist+diosgenin group.These results suggest that diosgenin alleviates the injury to and apoptosis of cardiomyocytes induced by CVB3,and that ERS inhibition may be the related molecular mechanism.
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