Gymnemic acid I triggers mechanistic target of rapamycin-mediated β cells cytoprotection through the promotion of autophagy under high glucose stress
| Autor: | Dongbo Liu, Yanyang Wu, Haiyan Zhou, Dengni lai, Yongquan Hu, Yushuang Luo, Zhongyi Tong, Yuju Yuan |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Physiology Clinical Biochemistry P70-S6 Kinase 1 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Cell Line Tumor Insulin-Secreting Cells Autophagy Animals Phosphorylation Mechanistic target of rapamycin PI3K/AKT/mTOR pathway biology TOR Serine-Threonine Kinases Cell Biology Saponins biology.organism_classification Cytoprotection Triterpenes Cell biology 030104 developmental biology Glucose chemistry 030220 oncology & carcinogenesis Ribosomal protein s6 Gymnemic acid biology.protein Gymnema sylvestre |
| Zdroj: | Journal of cellular physiology. 234(6) |
| ISSN: | 1097-4652 |
| Popis: | Gymnemic acid I (GA I) is a bioactive component of Gymnema sylvestre. It is an Indian traditional medicinal herb which has antidiabetic effect. However, the molecular mechanism is remaining to be elucidated. Here, we showed that high glucose promoted the rate of apoptosis, GA I decreased the apoptosis under the high glucose stress. Our further study explored that GA I increased the number of autophagosome and the ratio of light chain 3-I (LC3-I)/LC3-II in MIN-6 cells under the normal or high glucose stress by the methods of western blot analysis and immunofluorescence. It induced autophagy flux and inhibited the phosphorylation of mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase β-1 (p70 S6K/S6K1), which is a substrate of mTOR. GA I decreased the rate of apoptosis and the activity of caspase-3 under the high glucose stress. The inhibition of apoptosis and caspase-3 activity by GA I were increased after treating with autophagy inhibitor in mouse islet β cells MIN-6. Our data suggested that GA I-induced autophagy protected MIN-6 cells from apoptosis under high glucose stress via inhibition the phosphorylation activity of mTOR. |
| Databáze: | OpenAIRE |
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