{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T23:39:20Z","timestamp":1773013160279,"version":"3.50.1"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,4,26]],"date-time":"2025-04-26T00:00:00Z","timestamp":1745625600000},"content-version":"vor","delay-in-days":115,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Wilson\u2019s disease (WD) is an abnormal copper metabolism disease. GanDouFuMu decoction (GDFMD) is a traditional Chinese medicine, whicn has shown good therapeutic effects in clinical treatment of WD liver fibrosis;but its regulatory mechanism is still unclear.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    The serum of WD patients before and after GDFMD treatment were collected, the four items of liver fibrosis were detected by ELISA. The hepatic stellate cell (HSC) activities were assesed via CCK8 assay. The mRNA levels were evaluated by qPCR. The protein levels were checked by western blot. The autophygosomes were observed by transmission electron microscope (TEM). The transdifferentiation ability of HSCs into myofibroblasts was evaluated with anti\u2010\u03b1\u2010SMA antibody by immunofluorescence (IF). In copper\u2010laden rats with WD, the autophagy levels, and fibrosis level were observed by IF.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    The four items of liver fibrosis levels were decreased. GDFMD could increase the HSCs cell activity. GDFMD could increase miRNA\u201029b\u20103p levels, which was decreased by TGF\u2010\u03b21. miRNA\u201029b\u20103p inhibitors could reversed the suppression response of GDFMD on the the protein expression of ULK1, beclin1, LC3, \u03b1\u2010SMA, and Col1. GDFMD blocked the transdifferentiation of HSCs into myofibroblasts, inhibited liver fibrosis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    GDFMD blocked the transdifferentiation of HSCs into myofibroblasts by upregulating miRNA\u201029b\u20103p, and then inhibited liver fibrosis in WD.\n                  <\/jats:p>","DOI":"10.1155\/mi\/2776808","type":"journal-article","created":{"date-parts":[[2025,4,26]],"date-time":"2025-04-26T05:10:32Z","timestamp":1745644232000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanistic Insights Into GDFMD\u2010Mediated Inhibition of Liver Fibrosis via miRNA\u201029b\u20103p Upregulation in Wilson\u2019s 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