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Aims/Introduction  Non‐alcoholic steatohepatitis ( NASH ), which occurs in association with insulin resistance and hepatic fat accumulation, is characterized by chronic liver injury and fibrosis.  NASH  onset and progression is closely related to hepatic inflammation, which is partly regulated by the vagus nerve through the α7 nicotinic acetylcholine receptor (α7nAchR). Hepatic α7nAchR action is impeded in obesity and insulin resistance. In the present study, using α7nAchR knockout (α7 KO ) mice, we elucidated the effect of α7nAchR deficiency on  NASH ‐related inflammation and fibrosis.    Materials and Methods  α7 KO  mice were fed an atherogenic high‐fat diet ( AD ) for 32 weeks or methionine/choline‐deficient diet ( MCD ) for 6 weeks, both of which induce  NASH . Mice were then examined for the degree of  NASH ‐related inflammation and fibrosis by hepatic gene expression analysis and Sirius red histological staining.    Results  Hepatic triglyceride accumulation and elevated plasma transaminase levels were observed in both  AD  and  MCD  mice, but the plasma transaminase level increase was higher in α7 KO  mice than in control mice. α7 KO  mice fed an  AD  showed significant upregulation of the  Col1a1  gene encoding alpha‐1 type I collagen, which is involved in liver fibrosis, and the  Ccl2  gene encoding C‐C motif chemokine ligand 2, a pro‐inflammatory chemokine; α7 KO  mice fed an  MCD  had significant upregulation of the  Col1a1  gene and the  Tnf  gene, an inflammatory cytokine. Histological analysis showed that  AD  and  MCD  exacerbated liver fibrosis in α7 KO  mice.    Conclusions  The results of this study suggest that α7nAchR deficiency exacerbates hepatic inflammation and fibrosis in a diet‐induced mouse model of  NASH .

Nicotinic alpha‐7 acetylcholine receptor deficiency exacerbates hepatic inflammation and fibrosis in a mouse model of non‐alcoholic steatohepatitis