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| 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 |
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| Cite this article: |
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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.
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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.
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Received: 03 November 2021
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