右美托咪定通过抑制 AKT 和 ERK 减轻高糖诱导的 HK-2 上皮间质转化。
Dexmedetomidine Attenuates High Glucose-induced HK-2 Epithelial-mesenchymal Transition by Inhibiting AKT and ERK.
机构信息
Department of Anesthesiology, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin, China.
Department of Occupational and Environmental Health, School of Public Health, Jilin University, Changchun 130021, Jilin, China.
出版信息
Biomed Environ Sci. 2020 May 20;33(5):323-330. doi: 10.3967/bes2020.044.
OBJECTIVE
To explore the protective effects of dexmedetomidine (Dex) against high glucose-induced epithelial-mesenchymal transition in HK-2 cells and relevant mechanisms.
METHODS
HK-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.
RESULTS
Compared 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.
CONCLUSION
Dex can attenuate high glucose-induced HK-2 epithelial-mesenchymal transition by inhibiting AKT and ERK.
目的
探讨右美托咪定（Dex）对高糖诱导的 HK-2 细胞上皮间质转化的保护作用及其机制。
方法
将 HK-2 细胞分别用葡萄糖或葡萄糖+Dex 孵育 6 h，检测 ROS 产生、HK-2 细胞形态及细胞周期，并比较 HK-2 细胞在葡萄糖和葡萄糖+Dex 作用下，以及加入 PI3K/AKT 通路抑制剂 LY294002 和 ERK 通路抑制剂 U0126 前后 AKT、p-AKT、ERK、p-ERK、PI3K、E-Cadherin、Claudin-1 和α-SMA 的表达。
结果
与高糖组相比，高糖+Dex 组 HK-2 细胞 ROS 生成减少，细胞形态完整，G1 期细胞比例增加，p-AKT、p-ERK 和α-SMA 表达降低，E-Cadherin 和 Claudin-1 表达增加。PI3K/AKT 通路抑制剂 LY294002 和 ERK 通路抑制剂 U0126 降低了 p-AKT、p-ERK 和α-SMA 的表达，增加了 E-Cadherin 和 Claudin-1 的表达。
结论
Dex 可通过抑制 AKT 和 ERK 减轻高糖诱导的 HK-2 细胞上皮间质转化。
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