Oxidative Medicine and Cellular Longevity / 2020 / Article / Fig 3

Research Article

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

Figure 3

Role of AdipoRon in the expression of AdipoR1 and p-AMPK and ER stress in the kidneys of db/db mice. (a) Representative immunofluorescence images of AdipoR1 (A–C), GRP78 (D–F), and CHOP (G–I) in the renal tissues of three mouse groups. per group. . (b) Semiquantitative analysis of AdipoR1 and p-AMPK expression. (c) Semiquantitative analysis of nuclear CHOP positive cells (%). (d) Representative immunoblots of AdipoR1, p-AMPK, and T-AMPK. β-Actin was used as a loading control. (e) Relative band intensity. (f) Representative immunoblots of GRP78, p-PERK, PERK, and CHOP. (g) Relative band intensity. mice per group. The data are shown as the . versus db/m control mice; # versus db/db mice. AdipoR1: adiponectin receptor 1; GRP78: glucose-regulated protein of 78 kDa; CHOP: C/EBP homologous protein; p-AMPK: phosphorylated 5AMP-activated kinase; PERK: protein kinase-like endoplasmic reticulum kinase; p-PERK: phospho-PERK.

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