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