Figure 8: Resveratrol regulates autophagy and apoptosis in db/db mice and human podocytes through the suppression of miR-383-5p.

(a) The expression of miR-383-5p in db/m, db/db, and resveratrol-treated db/db mice. Data are the mean ± SEM of three experiments. *P < 0.05 vs. db/db. (b) The expression of miR-383-5p at different concentrations of resveratrol (0, 5, 10, and 15 μM) and HG (30 mM), NG (5.6 mM) in podocytes. Data are the mean ± SEM of three experiments. *P < 0.05 vs. HG (30 mM). (c) Podocytes were transfected with miR-383-5p mimics or Negative mimics. Twenty-four hours after transfection, the cells were treated with HG plus resveratrol (15 μM) for 48 h. Cell lysates were subjected to immunoblot analysis with antibodies for LC3, p62, Cleaved caspase-3, and Bax, with β-actin serving as a loading control. (d) Quantitative densitometry for LC3-II, Cleaved caspase-3, and Bax. Relative protein levels were normalized to that of β-actin. Data are the mean ± SEM of three experiments. *P < 0.05 vs. Negative mimics. (e) Podocytes were transfected with miR-383-5p inhibitors or Negative inhibitors. Twenty-four hours after transfection, the cells were treated with HG plus resveratrol (15 μM), bafilomycin A for 48 h. Cell lysates were prepared and subjected to immunoblot analysis with antibodies for LC3, p62, Cleaved caspase-3, and Bax, with β-actin serving as a loading control. (f) Quantitative densitometry for LC3-II, p62, Cleaved caspase-3, and Bax. Relative protein levels were normalized to that of β-actin. Data are the mean ± SEM of three experiments. *P < 0.05 vs. Negative inhibitors. ^#P < 0.05 vs. miR-383-5p inhibitors.