AdipoRon Protects against Tubular Injury in Diabetic Nephropathy by Inhibiting Endoplasmic Reticulum Stress

Figure 4

Effects of AdipoRon treatment on ER stress, inflammation, apoptosis, and fibrosis in HK-2 cells under HG conditions. (a) Representative confocal images of AdipoR1 in HK-2 cells treated or not treated with different concentrations of AdipoRon (5 μM, 10 μM, and 50 μM) under HG conditions. per group. . (b) Quantification of the average immunofluorescence intensity of AdipoR1 in HK-2 cells. (c) The levels of intracellular ROS in treated HK-2 cells as assessed by DCFH-DA staining. per group. . (d) Bars graphs depict intracellular ROS content in treated HK-2 cells. (e) Representative western blot bands of AdipoR1, p-AMPK, T-AMPK, GRP78, p-PERK, PERK, and CHOP in HK-2 cells treated with different concentrations of AdipoRon under HG conditions. β-Actin was used as a loading control. per group. (f) Relative band density of WB. (g) Immunoblot assays of Bcl-2, Bax, cleaved caspase 3, collagen I, and FN in treated HK-2 cells. per group. (h) mRNA levels of MCP-1, IL-6, and TNFα in HK-2 cells treated or not treated with different concentrations of AdipoRon (5 μM, 10 μM, and 50 μM) under HG conditions. per group. The data are shown as the . versus LG; ^# versus HG. LG: low glucose; HG: high glucose; ROS: reactive oxygen species; μM: μmol/L.

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