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. 2021 Jan 21;12(1):110. doi: 10.1038/s41419-020-03375-z

Fig. 2. Mas antagonist A779 prevented high-fat diet-induced autophagy, ER stress, and apoptosis in the cortex of kidneys in mice.

Fig. 2

A and B Representative immunoblots and corresponding densitometry analysis of Mas, LAMP1, P62, LC3B, BiP, CHOP, cleaved-caspase-3 and VDAC1 protein abundance in the kidney cortex of CTL, HFD, and HFD+A779 mice. C Representative photomicrographs of H&E, Masson staining and TUNEL staining the kidney of CTL, HFD, and HFD+A779 mice. Immunohistochemistry and immunofluorescence of LC3B, BiP, and VDAC1 in the kidney of CTL, HFD, and HFD+A779 mice. D mRNA levels of Mas, LC3B, BiP and VDAC1 in the kidney cortex of CTL, HFD, and HFD+A779 mice. E Representative images of mitochondria and endoplasmic reticulum by transmission electron microscopy (TEM) in proximal tubular cells prepared from HFD mice with or without A779 treatment. CTL, controls; HFD, high-fat diet; HFD+A779, high-fat diet plus A779 treatment. Data are shown as mean ± SEM; *P < 0.05 compared with CTL; #P < 0.05 compared with HFD.