Effects of ginkgolide B on Caspase-3/PTEN/Akt pathway and cell proliferation and apoptosis in hypoxia/reoxygenation cardiomyocytes
- VernacularTitle:银杏内酯B对缺氧/复氧心肌细胞Caspase-3/PTEN/Akt通路及细胞增殖凋亡的影响
- Author:
Haiyu CHEN
1
;
Fuzhen ZHENG
1
;
Guoxing WENG
1
;
Jiayin BAO
1
;
Jie HUANG
1
;
Licheng YAN
1
;
Qiuqing KE
2
Author Information
1. Department of Cardiovascular Surgery, Provincial Clinical School of Medicine, Fujian Medical University, Fujian Provincial Hospital, Fuzhou, 350001, P. R. China
2. Department of Internal Medicine, Provincial Clinical School of Medicine, Fujian Medical University, Fujian Provincial Jinshan Hospital, Fuzhou, 350001, P. R. China
- Publication Type:Journal Article
- Keywords:
Ginkgolide B;
hypoxia/reoxygenation;
cardiomyocyte;
Caspase-3/PTEN/Akt pathway;
cell proliferation;
cell apoptosis
- From:
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery
2022;29(12):1647-1652
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of ginkgolide B (GB) on cysteinyl aspartate specific proteinase-3 (Caspase-3)/chromosome 10 deletion phosphatase-tension protein homologue (PTEN)/protein kinase B (Akt) pathway and cell proliferation and apoptosis in hypoxia/reoxygenation cardiomyocytes. Methods H9C2 cells were cultured in vitro. A control group was cultured in serum-free DMEM high glucose medium at 37°C and 5% CO2 for 28 hours. The remaining groups were prepared with hypoxia/reoxygenation models. A GB low-dose group and a GB high-dose group were treated with GB pretreatment with final concentration of 50 μmol/L and 200 μmol/L respectively at 1 h before hypoxia/reoxygenation. A carvedilol group was treated with carvedilol of a final concentration of 10 μmol/L at 1 h before hypoxia/reoxygenation. The proliferation and apoptosis of H9C2 cells were detected, and the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), reactive oxygen species (ROS), PTEN, Akt, phosphorylated Akt (p-Akt) and Caspase-3 in H9C2 cells were also detected. Results Compared with the control group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in other groups decreased, and the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 increased (P<0.05). Compared with the hypoxia/reoxygenation group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in all GB dose groups and the carvedilol group increased; the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 decreased, and the effect of GB was in a dose dependent manner; however, the effect of GB was not as strong as carvedilol (P<0.05). Conclusion GB can inhibit H9C2 cell apoptosis and promote H9C2 cell proliferation by activating Caspase-3/PTEN/Akt pathway.
