Home > Browse Issues > Vol.37 No.11
Role of Resveratrol on High Glucose-induced Epithelial to Mesenchymal Transition of Human Renal Proximal Tubular Epithelial Cells
Wu Haijiang1, Deng Xinna2, Shi Yonghong1, Guo Qingjun1, Li Hongbo1, Peng Jinkai3, Pang Lei3, Cui Guipeng3, Duan Huijun1*
1Department of Pathology, Hebei Medical University, Key Laboratory of Kidney Diseases of Hebei Province,Shijiazhuang 050017, China;
2Department of Oncology & Immunotherapy, Hebei General Hospital, Shijiazhuang 050051, China;
3College of Basic Medical Hebei Medical University, Shijiazhuang 050017, China
2Department of Oncology & Immunotherapy, Hebei General Hospital, Shijiazhuang 050051, China;
3College of Basic Medical Hebei Medical University, Shijiazhuang 050017, China
Abstract: We investigated the role of resveratrol and SIRT1 signaling pathway on epithelial to mesenchymal transition of human renal proximal tubular epithelial cells (HK-2) cultured with high glucose. HK-2 cells were cultured in vitro. The protein levels of α-SMA， E-cadherin， SIRT1 and PGC-1α were determined by Western blot.The expression level of SIRT1 was also examined by immunofluorescence assay. Compared with 0 h， the exposure of HK-2 cells to high concentration of glucose resulted in decreased protein levels of SIRT1 in a time-dependent manner.But HK-2 cells incubated with low concentrations of glucose for various periods didn’t show a time-dependent decrease in SIRT1 expression. Resveratrol treatment resulted in increased protein level of SIRT1. This effect was markedly diminished by the addition of EX527， an inhibitor of SIRT1. Furthermore， resveratrol treatment also resulted in increased protein level of E-cadherin， along with a down-regulation of α-SMA， although EX527 alone had no effect on high glucose-induced EMT of HK-2 cells. In addition， resveratrol treatment also prevented the decrease of PGC-1α in HK-2 cells cultured with high glucose. Taken together， these data demonstrated that resveratrol could prevent high glucose-induced EMT of human renal proximal tubular epithelial cells via activation of SIRT1 and PGC-1α signaling pathway.
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