ADSCs attenuate Liver fibrosis via inducing HSC senescence: validation in dual-etiology models.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Liver fibrosis (LF) results from various causes, which require finding conserved mechanisms to help treat related diseases. Although adipose-derived stem cells (ADSCs) transplantation can alleviate hepatic fibrosis, their mechanism remains unclear. Accordingly, we explored the efficacy and mechanisms behind ADSCs transplantation in two LF models. Methodology The carbon tetrachloride (CCl4)-induced liver injury and Echinococcus multilocularis (E. multilocularis) infection models were established, and ADSCs were transplanted. Mouse liver samples were harvested and analyzed histologically. Expression levels of fibrosis and senescence-related proteins were analyzed by immunohistochemistry. Hepatic stellate cells (HSCs) activation and cell senescence protein expression were evaluated via western blotting. Co-localization expression was determined by immunofluorescence. To assess the cellular senescence degree, we utilized senescence-associated β-galactosidase (SA-β-Gal) staining. Result In the CCl4-induced LF mouse model, the liver surface exhibited a rough texture. The hematoxylin and eosin (H&E) staining revealed hepatic parenchymal cell destruction accompanied by pseudolobule formation and fibrosis in the portal area. In the E. multilocularis infection model, multiple white foci were on the liver surface. The H&E staining revealed massive inflammatory cell infiltration

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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