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In this study, the role of miR\u2010193a\/b\u20103p in concanavalin A (ConA)\u2010induced liver fibrosis in mice was evaluated. According to the results, the expression of miR\u2010193a\/b\u20103p was down\u2010regulated in liver tissues after exposure to ConA. Lentivirus\u2010mediated overexpression of miR\u2010193a\/b\u20103p reduced ConA\u2010induced liver injury as demonstrated by decreasing ALT and AST levels. Moreover, ConA\u2010induced liver fibrosis was restrained by the up\u2010regulation of miR\u2010193a\/b\u20103 through inhibiting collagen deposition, decreasing desmin and proliferating cell nuclear antigen (PCNA) expression and lessening the content of hydroxyproline, transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21) and activin A in liver tissues. Furthermore, miR\u2010193a\/b\u20103p mimics suppressed the proliferation of human HSCs LX\u20102 via inducing the apoptosis of LX\u20102 cells and lowering the levels of cell cycle\u2010related proteins Cyclin D1, Cyclin E1, p\u2010Rb and CAPRIN1. Finally, TGF\u2010\u03b21 and activin A\u2010mediated activation of LX\u20102 cells was reversed by miR\u2010193a\/b\u20103p mimics via repressing COL1A1 and \u03b1\u2010SMA expression, and restraining the activation of TGF\u2010\u03b2\/Smad2\/3 signalling pathway. CAPRIN1 and TGF\u2010\u03b22 were demonstrated to be the direct target genes of miR\u2010193a\/b\u20103p. We conclude that miR\u2010193a\/b\u20103p overexpression attenuates liver fibrosis through suppressing the proliferation and activation of HSCs. Our data suggest that miR\u2010193a\u20103p and miR\u2010193b\u20103p may be new therapeutic targets for liver fibrosis.<\/jats:p>","DOI":"10.1111\/jcmm.14210","type":"journal-article","created":{"date-parts":[[2019,4,4]],"date-time":"2019-04-04T04:10:53Z","timestamp":1554351053000},"page":"3824-3832","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["miR\u2010193a\/b\u20103p relieves hepatic fibrosis and restrains proliferation and activation of hepatic stellate cells"],"prefix":"10.1111","volume":"23","author":[{"given":"Baoling","family":"Ju","sequence":"first","affiliation":[{"name":"Department of Immunology Mudanjiang Medical College Mudanjiang Heilongjiang People's Republic of China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ying","family":"Nie","sequence":"additional","affiliation":[{"name":"Department of Immunology Mudanjiang Medical College Mudanjiang Heilongjiang People's Republic of 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