Gymnemic acid I triggers mechanistic target of rap...
Yanyang Wu1，2，3 Yongquan Hu2，4，5 Yuju Yuan1，2，3 Yushuang Luo2，4，5 Dengni Lai1，2，3 Haiyan Zhou2，4，5 Zhongyi Tong6 Dongbo Liu2，4，5
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；(https://www.daowen.com)
5.State Key Laboratory of Subhealth Intervention Technology，Changsha，China；
6.Department of Pathology，The Second Xiangya Hospital of Central South University，Changsha，China
Abstract：Gymnemic acid I(GA I)is a bioactive component of Gymnemasylvestre.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-Ⅱin 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(m TOR)and ribosomal protein S6 kinaseβ-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 isletβ-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