Effects of Rg_1 on LPS-induced apoptosis and autophagy of lung epithelial cells.
10.19540/j.cnki.cjcmm.20190111.002
- Author:
Qi-Jian JI
1
;
Zhao-Rui SUN
2
;
Zhi-Zhou YANG
2
;
Wei ZHANG
2
;
Yi REN
2
;
Li-Ping CAO
2
;
Liang LI
2
;
Shi-Nan NIE
2
Author Information
1. Department of Emergency Medicine,Jinling Clinical Medical College,Nanjing Medical University Nanjing 210002,China Department of Critical Care Medicine,People's Hospital of Xuyi County Xuyi 211700,China.
2. Department of Emergency Medicine,Jinling Clinical Medical College,Nanjing Medical University Nanjing 210002,China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
autophagy;
ginsenosides Rg1;
lung injury;
sepsis
- MeSH:
Animals;
Apoptosis;
Autophagy;
Cells, Cultured;
Epithelial Cells;
drug effects;
Ginsenosides;
pharmacology;
Lipopolysaccharides;
Lung;
cytology;
Mice
- From:
China Journal of Chinese Materia Medica
2019;44(8):1648-1653
- CountryChina
- Language:Chinese
-
Abstract:
This paper aimed to study the protective effect of ginsenoside Rg_1 on endotoxin(LPS)-induced apoptosis of lung epithelial cells and its mechanism of action. Mouse lung epithelial cells(MLE-12) were first treated with LPS. The autophagy changes and apoptosis and the relationship with concentration and time of LPS were observed. Then,the level of autophagy in MLE-12 was regulated at a specific concentration and action time of LPS,and the changes of apoptosis were observed. Secondly,ginsenoside Rg_1 and autophagy inhibitor 3-MA were added respectively at the same concentration and action time of LPS. The lung epithelial cells were grouped to observe the effect of ginsenoside Rg_1 on LPS-induced apoptosis of lung epithelial cells and its mechanism. In the animal experiment,the mice were grouped and tested by apoptosis protein,lung injury score and HE staining section to verify whether ginsenoside Rg_1 has a protective effect on LPS-induced lung injury. The results showed that apoptosis and autophagy increased as the rise of concentration after treatment with LPS for 12 h. The apoptosis increased gradually,and the autophagy increased first and then decreased over time at the LPS concentration of 25 g·L-1. The apoptosis of LPS group was higher than that of control group,and LPS+3-MA group increased further,while apoptosis decreased significantly in LPS+RAM(rapamycin,autophagy promoter) group. The autophagy increased in LPS group,decreased in LPS+3-MA group and increased in LPS+RAM group. The apoptosis of LPS group was higher than that of control group,and the apoptosis of LPS+Rg_1 group decreased. The apoptosis of LPS+Rg_1+3-MA group increased again. The autophagy of LPS group further increased after administration of ginsenoside Rg_1,but decreased after administration of 3-MA. In the in vivo experiments in mice,the apoptosis of LPS group increased significantly compared with the control group,while LPS + ginsenoside Rg_1 group decreased. Lung injury score and HE staining also conformed to the above trend. LPS can induce the apoptosis of lung epithelial cells in a time-dependent and concentration-dependent manner. The autophagy of lung epithelial cells increases with the rise of LPS concentration. At the specific concentration of LPS,autophagy increases first and then decreases after 12-16 hours. Proper increase of autophagy in lung epithelial cells within a certain period of time can reduce the apoptosis induced by LPS,while inhibition of autophagy can increase apoptosis. Ginsenoside Rg_1 has a protective effect on lung cancer epithelial cell apoptosis induced by autophagy.
