Dexmedetomidine Attenuates High Glucose-induced HK-2 Epithelial-mesenchymal Transition by Inhibiting AKT and ERK |
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Institution: | 1. Department of Anesthesiology, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin, China;2. Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun 130021, Jilin, China;3. Department of Ultrasound, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin, China |
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Abstract: | ObjectiveTo explore the protective effects of dexmedetomidine (Dex) against high glucose-induced epithelial-mesenchymal transition in HK-2 cells and relevant mechanisms.MethodsHK-2 cells were exposed to either glucose or glucose+Dex for 6 h. The production of ROS, morphology of HK-2 cells, and cell cycle were detected. Moreover, the expression of AKT, p-AKT, ERK, p-ERK, PI3K, E-Cadherin, Claudin-1, and α-SMA were determined and compared between HK-2 cells exposed to glucose and those exposed to both glucose and Dex with or without PI3K/AKT pathway inhibitor LY294002 and ERK pathway inhibitor U0126.ResultsCompared with HK-2 cells exposed to high level of glucose, the HK-2 cells exposed to both high level of glucose and Dex showed: (1) lower level of ROS production; (2) cell morphology was complete; (3) more cells in G1 phase; (4) lower expression of p-AKT, p-ERK and α-SMA, higher expression of E-Cadherin and Claudin-1. PI3K/AKT inhibitor LY294002 and ERK inhibitor U0126 decreased the expression of p-AKT, p-ERK and α-SMA, and increased the expression of E-Cadherin and Claudin-1.ConclusionDex can attenuate high glucose-induced HK-2 epithelial-mesenchymal transition by inhibiting AKT and ERK. |
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Keywords: | Dexmedetomidine Epithelial-mesenchymal transition High glucose Oxidative stress HK-2 cells |
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