Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Effect of dexmedetomidine on AKT/ERK signaling pathway and EMT-related proteins in high glucose-induced apoptosis in human renal tubular epithelial cells

Shuhua Wei¹ , Jiang Wu², Yubo Liu¹, Xiang He¹,

¹Department of Anesthesiology, Jiangxi General Hospital of Armed Police Force, Nanchang City; ²Department of Anesthesiology, 909 Hospital of Joint Logistics Support Force, Zhangzhou City, China.

For correspondence:- Shuhua Wei Email: fctyh9@163.com

Accepted: 7 March 2021 Published: 31 March 2021

Citation: Wei S, Wu J, Liu Y, He X, Effect of dexmedetomidine on AKT/ERK signaling pathway and EMT-related proteins in high glucose-induced apoptosis in human renal tubular epithelial cells. Trop J Pharm Res 2021; 20(3):537-541 doi: 10.4314/tjpr.v20i3.14

© 2021 The authors.
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Abstract

Purpose: To study the effect of dexmedetomidine (Dex) on AKTERK signaling pathway and EMT-related proteins in high glucose-induced apoptosis in human kidney tubular epithelial cells.

Methods: HK-2 cells were assigned to control, high-glucose and Dex groups. Levels of ROS were determined using live cell station. Flow cytometry was used to measure cell apoptosis and cell cycle while Western blot was applied to assay levels of PI3K, Akt, p-Akt, ERK and p-ERK.

Results: The ROS concentrations were markedly reduced in Dex group, relative to high glucose group (p < 0.05). Apoptosis was reduced in Dex group, relative to high glucose group, while P13K protein levels were significantly lower in high glucose and Dex groups than their corresponding control levels. In the high glucose-treated cells, AKT protein expression was downregulated, relative to control group, and p-AKT expression was markedly reduced in Dex group (p < 0.05). Protein expressions of ERK and p-ERK in high glucose group were lower than control values, but were significantly accentuated in Dex group, relative to high glucose group (p < 0.05).

Conclusion: Dex mitigates high glucose-induced apoptosis of HK-2 cells, increases the proportion of cells in G1 phase, and reduces their EMT via a mechanism related to regulation of AKTERK signaling pathway-associated proteins. AKTERK signaling pathway-associated proteins provide insights into the development of drugs for the treatment of diabetic nephropathy.

Keywords: Dexmedetomidine, High glucose, Human renal tubular epithelial cells, AKTERK signaling pathway, EMT-related proteins