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However, the effect of CE on liver natural killer (NK) cells and the potential of transforming growth factor-\u03b2 (TGF-\u03b2) signalling inhibition on alleviating CE-related liver damage remain to be explored. Here, by using the CE-mouse model, we revealed that the inhibitory receptors on the surface of liver NK cells were up-regulated, whereas the activating receptors were down-regulated over time. TGF-\u03b21 secretion was elevated in liver tissues and mainly derived from macrophages. A combination of TGF-\u03b2 signalling inhibitors SB525334 and pirfenidone could reduce the expression of TGF-\u03b21 signalling pathway-related proteins and collagen production. Based on the secretion of TGF-\u03b21, only the pirfenidone group showed a depressing effect. Also, the combination of SB525334 and pirfenidone exhibited a higher potential in effectively alleviating the senescence of the hepatocytes and restoring liver function. Together, TGF-\u03b21 may be a potential target for the treatment of CE-associated liver fibrosis.<\/jats:p>","DOI":"10.1017\/s0031182021000287","type":"journal-article","created":{"date-parts":[[2021,2,15]],"date-time":"2021-02-15T02:44:50Z","timestamp":1613357090000},"page":"767-778","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":11,"title":["A combination of pirfenidone and TGF-\u03b2 inhibition mitigates cystic echinococcosis-associated hepatic 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