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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Hepatology. 2011 Dec;54(6):2208–2217. doi: 10.1002/hep.24646

Fig. 1. Activation of LXR in transgenic mice conferred resistance to APAP hepatotoxicity.

Fig. 1

(A) Schematic representation of the Fabp-VP-LXRα transgene and confirmation of transgene expression by Northern blot analysis. Membrane was probed with a LXRα cDNA probe. Each lane represents RNA samples pooled from five mice of the same genotype. Fabp, rat fatty acid binding protein; SV40, SV40 poly(A) sequences; Tg, transgenic; VP, viral protein 16; Wt, wild type. (B) Representative H&E staining on liver paraffin sections of the vehicle-treated mice. (C) Representative H&E staining on liver paraffin sections of APAP-treated mice. APAP-induced centrilobular necrosis is indicated by arrows. C-c and C-d are higher magnifications of the framed fields in C-a and C-b, respectively. (D) Serum levels of AST, ALT, total bilirubin, and alkaline phosphatase in mice treated with APAP. *, P<0.05; **, P<0.01.