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자료유형
학술저널
저자정보
Hanh Nguyen Dong (Kangwon National University) 박소영 (Kangwon National University) Cong Thuc Le (Kangwon National University) 최대희 (강원대학교 의학전문대학원 내과학교실) 조은희 (강원대학교)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.35 No.3
발행연도
2020.1
수록면
647 - 655 (9page)

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Background: Hepatic stellate cells (HSCs) are known to play a fundamental role in the progression of liver fibrosis. Once HSCs areactivated, they are involved in proliferation, migration, and contractility which are characteristics of liver fibrogenesis. Recent studies have shown that irisin, a myokine secreted during physical exercise, has a protective effect in various metabolic diseases, especially in renal fibrosis. However, whether irisin is involved in HSC activation and other processes associated with liver fibrosis hasnot yet been investigated. In this study, we reveal the role of irisin in HSC activation as well as in proliferation, migration, and contractile properties of HSCs in vitro. Methods: LX-2 cells, immortalized human HSCs, were treated with transforming growth factor beta 1 (TGF-β1), a core regulator ofHSC fibrosis, with or without irisin, and markers of the aforementioned processes were analyzed. Further, an inflammatory responsewas stimulated with TGF-β1 and lipopolysaccharide (LPS) in combination with irisin and the expression of cytokines was measured. Results: Recombinant irisin significantly suppressed the expression of TGF-β1-stimulated fibrosis markers including alpha-smoothmuscle actin and collagen type 1 alpha 1 and prevented the TGF-β1-induced proliferation, migration, and contractility of LX-2 cells. Additionally, irisin ameliorated the production of interleukin-6 (IL-6) and IL-1β induced by TGF-β1 and LPS treatments. Conclusion: These findings suggested that irisin potently improved the progression of hepatic fibrosis by regulating HSC activation,proliferation, migration, contractility, and HSC-mediated production of inflammatory cytokine.

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