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. 2018 Dec 6;21:101068. doi: 10.1016/j.redox.2018.101068

Fig. 7.

Fig. 7

Overexpression of hepatic Nrf2 expression functionally restored the liver injury induced by adropin-deficiency in mice. WT and Adropin-KO male mice fed MCD for 4 weeks. AAV8-GFP and AAV8–Nrf2 vectors were administered following the initiation of MCD feeding. (A) H&E, Sirius Red, Oil Red O, and DHE staining of liver sections (magnification, ×200), scale bar: 200 µm. (B-E) Hepatic histological analysis of H&E staining. (F) Quantitative analysis of Sirius Red staining. (G) Hepatic TG contents. (H) Quantitative analysis of DHE staining. (I) Serum ALT and AST levels. (J) The mRNA expression of Col1a1, Acta2, Il1b, Il6 and Tnf in the liver. (K-L) Cleaved caspase-3 expression of total liver lysates. (M) The liver MDA levels. (N) The liver GSH levels. (O) The mRNA expression of Fasn, Acaca, Scd1, Cpt1a, Acadm and Cd36. (H, J, L, O) WT/GFP group was set as 1. The data are expressed as the mean ± SD, n = 8, * P < 0.05 wt/GFP versus Adropin-KO/GFP; #P < 0.05 Adropin-KO/GFP versus Adropin-KO/Nrf2.