Oxidative stress induces autophagy to inhibit the proliferation and apoptosis of human bone marrow mesenchymal stem cells (hBMSCs).
- Author:
Zhijun LIU
1
;
Shaojin LIU
2
;
Weipeng ZHENG
1
;
Hewei WEI
3
;
Zhihao LIAO
1
;
Sheng CHEN
1
Author Information
1. Department of Sports Medicine, The Third Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510240, China.
2. Department of Sports Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510115, China.
3. Department of Sports Medicine, The Third Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510240, China. *Corresponding author, E-mail: whwhou@163.com.
- Publication Type:Journal Article
- MeSH:
Humans;
Beclin-1/metabolism*;
Caspase 3/metabolism*;
Reactive Oxygen Species/metabolism*;
Hydrogen Peroxide/pharmacology*;
Apoptosis;
TOR Serine-Threonine Kinases/metabolism*;
Oxidative Stress;
Autophagy;
Mesenchymal Stem Cells/metabolism*;
Cell Proliferation
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(7):626-632
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of H2O2-induced oxidative stress on autophagy and apoptosis of human bone marrow mesenchymal stem cells (hBMSCs). Methods hBMSCs were isolated and cultured. The cells were divided into control group, 3-MA group, H2O2 group, H2O2 combined with 3-MA group. DCFH-DA staining was used to analyze the level of reactive oxygen species (ROS). hBMSCs were treated with 0, 50, 100, 200, 400 μmol/L H2O2, and then the cell viability was detected by CCK-8 assay. The level of autophagy was detected by monodansylcadaverine (MDC) staining and LysoTracker Red staining. The cell apoptosis was detected by flow cytometry. Western blotting was used to detect the expression of beclin 1, mTOR, phosphorylated mTOR (p-mTOR), cleaved caspase-3(c-caspase-3) and caspase-3 proteins. Results Compared with the control group and 3-MA group, ROS level and autophagosomes were increased and the proliferation and apoptosis were decreased in H2O2 group. The protein expression of beclin 1, mTOR, c-caspase-3 was up-regulated, while the p-mTOR was down-regulated. Compared with the 3-MA group, the H2O2 combined with 3-MA group also had an increased ROS level and autophagosomes, but not with significantly increased apoptosis rate; The protein expression of beclin 1, mTOR, c-caspase-3 was up-regulated, and the p-mTOR was down-regulated. Conclusion H2O2 can induce hMSCs to trigger oxidative stress response. It enhances the autophagy and inhibits the proliferation and apoptosis of hBMSCs.
