Objective To study the effect of IL-22 on the colonic barrier and its relationship with Nrf2 pathway in liver fibrosis mice.Methods The mice were divided into four groups:the control group(CON group),the model group(MOD group),the interleukin-22 group(IL-22 group),and the IL-22+ML385 group(ML385,an inhibitor of Nrf2),with 10 mice in each group,and the modeling cycle was 8 weeks.Liquid feed containing alcohol and carbon tetrachloride olive oil were given intraperitoneally in all groups except the CON group;IL-22 was given on top of this in the IL-22 group;and ML385 was injected intraperitoneally in the IL-22+ML385 group one hour before IL-22 treatment.At the end of modeling,the livers were stained with HE and Masson staining to clarify whether fibrosis occurred in the mice;the feces were collected to detect the cocci to bacillus ratio and observe the growth of intestinal flora;the colons were stained with HE staining,immunofluorescence and immunohistochemistry,and analyzed for the expression of tight junction proteins ZO-1,Occludin,and the Nrf2 pathway proteins(Nrf2,HO-1,and NQO1).The expression of these proteins was analyzed by immunohistochemistry.Results Compared with the CON group,mice in the MOD group showed significant fibrosis in the liver tissue,inflammatory cell infiltration in the colon tissue,and decreased expression of tight junction proteins(P<0.05).No overgrowth of various pathogenic bacteria was seen in fecal media.And there was no significant difference in the bulb-to-bar ratio.Compared with the MOD group,both liver and colon histopathologic damage were reduced in the IL-22 group,and tight junction protein expression was elevated,in addition,the expression levels of Nrf2,NQO1,and HO-1 were also elevated(P<0.05),whereas there was no significant change in the IL-22+ML385 group.Conclusion IL-22 improved the colonic barrier function in liver fibrosis mice,and the mechanism was related to the activation of Nrf2 anti-oxidative stress pathway.

AIM: To investigate the effect of FAK - related non - kinase ( FRNK) on the expression of membrane - type matrix metalloproteinase -1 ( MT1 - MMP) in hepatic stellate cells ( HSC). METHODS:FRNK were trans-fected into HSCs by cationic liposome method. The protein levels of FRNK in HSC were assayed by Western blotting. The levels of MT1 - MMP were determined by RT - PCR for mRNA and by Western blotting for protein, respectively. RESULTS: The up -regulated expression of FRNK protein was observed and it was at 48 h after transfection that the FRNK protein content was the highest ( P < 0.05 ). The expressions of MT1 - MMP mRNA and protein were also up - regulated by the transfection of FRNK, and it was at 48 h after transfection that the MT1 - MMP protein content was significantly increased. CONCLUSION: The mRNA and protein of FRNK were over - expressed in HSC transfected with the gene of FRNK. The inhibitory effect of FRNK on the collagen synthesis in HSC may be through the up - regulation of MT1 - MMP.