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Antioxidant Peptide SS-31 Inhibits High Glucose Induced Cardiomyocyte Apoptosis


LI Yu1, CHEN Zhihao1, TANG Lijuan2*, LIANG Zihui3, CHEN Juan4

(1Xiang’an Hospital Affiliated to Xiamen University, Xiamen 361102, China; 2Hebei Provincial Center for Disease Control and Prevention, Institute of Chronic Non-communicable Diseases, Shijiazhuang 050021, China; 3Hebei Medical University, Department of Clinical Practice Teaching, Shijiazhuang 050000, China; 4Hebei University of Economics, Economic Management College Hospital, Shijiazhuang 050000, China)
Abstract:

The aim of this article was to investigate the effect of antioxidant peptide SS-31 on HG (high glucose)-induced apoptosis in rat cardiomyocytes. In vitro culture of rat cardiomyocytes (H9C2) were stimulated with high glucose (30 mmol/L), and treated with antioxidant peptide SS-31. The protein expressions of Bax, Bcl2, Cleaved caspase-3, Nox1, Nox4 and Txnip were observed by Western blot. The mRNA expressions of Bax, Bcl2, Nox1, Nox4 and Txnip were observed by Real-time PCR. The nick end labeling method (TUNEL) was used to observe the apoptotic H9C2 cells situation. MitoSOXTM Red staining was used to detect the production of mitochondrial ROS in H9C2 cells. Compared with the normal control group, the apoptosis of H9C2 cells, was significantly increased. The proteins expression of Bax, Cleaved caspase-3, Nox1, Nox4 and Txnip was up-regulated. The expression of Bcl-2 protein was decreased, and the production of mitochondrial ROS was increased in high glucose stimulated H9C2 cells. Treatment with SS-31 could inhibit the apoptosis of H9C2 cells, down-regulating the expression of Bax, Cleaved caspase-3, Nox1, Nox4 and Txnip, up-regulating the expression of Bcl-2 and reduce the production of mitochondrial ROS in high glucose induced H9C2 cells. Above mentioned results suggest that SS-31 inhibits HG-induced rat cardiomyocytes apoptosis and TXNIP/ROS production, indicating that antioxidant peptide SS-31 may have a certain improvement effect on diabetic cardiomyopathy.


CSTR: 32200.14.cjcb.2020.04.0010