Dexmedetomidine Attenuates High Glucose-induced HK-2 Epithelial-mesenchymal Transition by Inhibiting AKT and ERK.
- Author:
Qi Zheng PAN
1
;
Kai LI
1
;
Zhuo Dong YANG
2
;
Ming GAO
1
;
Jia Hong SHI
3
;
Shu Ping REN
2
;
Guo Qing ZHAO
1
Author Information
- Publication Type:Journal Article
- Keywords: Dexmedetomidine; Epithelial-mesenchymal transition; HK-2 cells; High glucose; Oxidative stress
- MeSH: Adrenergic alpha-2 Receptor Agonists; pharmacology; Cell Line; Dexmedetomidine; pharmacology; Epithelial-Mesenchymal Transition; drug effects; Glucose; metabolism; Humans; MAP Kinase Signaling System; drug effects; Proto-Oncogene Proteins c-akt; antagonists & inhibitors; Signal Transduction; drug effects
- From: Biomedical and Environmental Sciences 2020;33(5):323-330
- CountryChina
- Language:English
-
Abstract:
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.
