Protective effect of Hirsutine on H2O2-induced oxidative stress injury in rat cardiomyocytes and its mechanisms
DING Lu1, 2, MA Luoping1, MENG Mingxing1, WANG Lei3, JIANG Sheng3, GUAN Zhimin1,ZHANG Tingcai1, LI Na4
1.Department of Medicine, Hubei University of Arts and Science, Xiangyang 441053,China; 2.School of Basic Medicine, Wenzhou Medical University, Wenzhou 325035, China; 3.Department of Cardiac Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China;4.Department of Science and Education, People's Hospital of Weifang High-tech Zone, Weifang 261000, China
DING Lu,MA Luoping,MENG Mingxing, et al. Protective effect of Hirsutine on H2O2-induced oxidative stress injury in rat cardiomyocytes and its mechanisms[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2022, 52(1): 51-56.
Abstract：Objective: To investigate whether Hirsutine has protective effect on H2O2-induced oxidative stress injury in rat cardiomyocytes and its possible mechanisms. Methods: Primary neonatal rat cardiomyocytes,extracted from 1-2 days old neonatal rats, were stimulated with 400 μmol/L H2O2 to replicate the oxidative stress cell model. Cells were divided into 4 groups: Control, HS, H2O2, H2O2+HS. Cell activity, cell apoptosis and cell morphology were respectively detected by CCK8 assay, Tunel assay and immunofluorescence. Protein level of Bcl-2, Bax, Caspase-3 and Cleaved- caspase-3 was detected by Western blot. Results: It was found that the cell viability was significantly decreased after 6, 12, 24 hours of H2O2 treatment (P<0.01), compared with Control group, but it was significantly increased by 1 μmol/L and 10 μmol/L Hirsutine (P<0.01) compared with H2O2 group; Compared with H2O2 group, cell viability did not change and was markedly decreased by 100 μmol/L Hirsutine (P<0.01). Compared with H2O2 group, H2O2+HS group had significant increase in the apoptosis of cells (P<0.05) and the sarcomere structure was relatively intact. Compared with H2O2 group, the level of Bax/Bcl-2 and Cleaved-caspase 3/Caspase 3 was decreased by Hirsutine treatment, and Nrf2 and HO-1 protein increased by Hirsutine treatment (P<0.05). Conclusion: Hirsutine had protective effect on H2O2-induced mitochondrial apoptosis of rat cardiomyocytes, which may be mediated by Nrf2-HO-1 signaling pathway.
