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.
 
 
 
Highlights
Diabetic nephropathy (DN) is a chronic metabolic disorder caused by deficiency in insulin secretion and/or dysfunction in insulin action
There was reduced number of cells in G1 phase in high glucose group, relative to control, while G1 phase cells were higher in Dex group than in high glucose-treated cells (p < 0.05)
The cell morphology of the Dex group was good, and cell density was significantly higher than that in cells treated with high-glucose, but lower than control value, while ROS levels in cells exposed to high glucose were markedly higher than control values
Summary
Diabetic nephropathy (DN) is a chronic metabolic disorder caused by deficiency in insulin secretion and/or dysfunction in insulin action. It occurs frequently in diabetic patients, and it is a serious microvascular disease that can lead to kidney failure and end-stage renal disease [1]. Recent studies have found that the incidence of DN is increasing year by year, thereby seriously endangering the life and health of patients [2]. The pathogenesis of DN is not completely clear. It has been reported that the occurrence of DN is closely related to EXPERIMENTAL Materials. Human renal cortex proximal convoluted tubule epithelial cells (HK-2 cells) were provided by Wuhan Yipu Biotechnology Co. Ltd
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