2. Academic Validation
  3. Gymnemic acid I triggers mechanistic target of rapamycin-mediated β cells cytoprotection through the promotion of autophagy under high glucose stress

Gymnemic acid I triggers mechanistic target of rapamycin-mediated β cells cytoprotection through the promotion of autophagy under high glucose stress

  • J Cell Physiol. 2019 Jun;234(6):9370-9377. doi: 10.1002/jcp.27621.
Yanyang Wu 1 2 3,  Yongquan Hu 2 4 5,  Yuju Yuan 1 2 3,  Yushuang Luo 2 4 5,  Dengni Lai 1 2 3,  Haiyan Zhou 2 4 5,  Zhongyi Tong 6,  Dongbo Liu 2 4 5
Affiliations

Affiliations

  • 1 Hunan Agricultural University, Changsha, China.
  • 2 Horticulture and Landscape College, Hunan Agricultural University, Changsha, China.
  • 3 College of Food Science and Technology, Hunan Agricultural University, Changsha, China.
  • 4 Hunan Co-Innovation Center for Utilization of Botanical Functional Ingredients, Changsha, China.
  • 5 State Key Laboratory of Subhealth Intervention Technology, Changsha, China.
  • 6 Department of Pathology, The Second Xiangya Hospital of Central South University, Changsha, China.
PMID: 30370588 DOI: 10.1002/jcp.27621
Abstract

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.

Keywords

apoptosis; autophagy; gymnemic acid; high glucose.

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