Dexmedetomidine Attenuates High Glucose-induced HK-2 Epithelial-mesenchymal Transition by Inhibiting AKT and ERK / 生物医学与环境科学(英文)
Biomedical and Environmental Sciences
;
(12): 323-330, 2020.
Article
in English
| WPRIM
| ID: wpr-829009
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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Signal Transduction
/
Cell Line
/
Dexmedetomidine
/
MAP Kinase Signaling System
/
Proto-Oncogene Proteins c-akt
/
Adrenergic alpha-2 Receptor Agonists
/
Epithelial-Mesenchymal Transition
/
Glucose
/
Metabolism
Limits:
Humans
Language:
English
Journal:
Biomedical and Environmental Sciences
Year:
2020
Type:
Article
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