Fig. 3: Hepatic GABAARγ2 upregulation in response to hepatic lipoanabolism determined by immunohistochemistry. | Cell Death & Disease

Fig. 3: Hepatic GABAARγ2 upregulation in response to hepatic lipoanabolism determined by immunohistochemistry.

From: Inhibition of acyl-CoA binding protein (ACBP) by means of a GABAARγ2-derived peptide

Fig. 3: Hepatic GABAARγ2 upregulation in response to hepatic lipoanabolism determined by immunohistochemistry.The alternative text for this image may have been generated using AI.

A Experimental design. C57BL/6 male mice were fed with RCD, WD, and methionine/choline-deficient diet (MCD) over the course of 6 weeks. B Representative images of hepatic hematoxylin and eosin (HE), and GABAARγ2 immunohistochemistry (IHC) staining from mice fed with RCD, WD or MCD (n = 5 mice per condition), non-alcoholic fatty liver disease (NAFLD) activity score quantification (C). Hepatic GABAARγ2quantification (expressed as % percentage of GABAARγ2 -positive cells) in liver parenchyma (D) and peri-central / periportal vein (E) areas. Results are displayed as whisker plots with each dot representing one single mouse (n = 5 mice per condition) including the means ± SEM. For statistical analyses, p values are calculated by two-tailed unpaired Mann–Whitney U-test (C) or one-way ANOVA (D, E).

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