Sch B，一种从五味子（Schisandrae chinensis (Turcz.) Baill. （五味子科）的果实中提取出的活性成分，具有多种药理活性，包括抗肿瘤、抗炎和肝脏保护作用。本研究旨在探讨Sch B对肝纤维化中活化的HSC细胞衰老的影响及其机制。使用CCl4诱导的肝纤维化的ICR小鼠补充40mg/kg的Sch B，持续30天，用5μM，10μM和20μM浓度的Sch B处理LX2细胞24小时，通过衰老相关指标衰老相关β-半乳糖苷酶（SA-β-gal）活性和p16、p21、p53、γ-H2AX、H3K9me3、TERT、TRF1和TRF2的表达评估细胞衰老。使用铁铵柠檬酸盐（FAC）和NCOA4 siRNA评估Sch B调控细胞衰老的机制。结果表明，Sch B（40mg/kg）降低了小鼠血清AST和ALT的水平（53.2%和63.6%），减轻了肝胶原沉积，并促进了激活的HSC细胞衰老。用20μM的Sch B处理细胞导致细胞存活率下降到80.38±4.87%，促进SA-β-gal活性，p16、p21和p53的水平分别增加了4.5倍、2.9倍和3.5倍，TERT、TRF1和TRF2的水平分别下降了2.4倍、2.7倍和2.6倍。FAC（400μM）增强了上述Sch B的效应。NCOA4 siRNA削弱了Sch B对铁沉积和HSC细胞衰老的作用。Sch B可能通过促进活化的HSC细胞衰老来改善肝纤维化，这可能归因于其诱导NCOA4介导的铁蛋白噬菌体及随后的铁过载。

Schisandrin B (Sch B), an active ingredient from Schisandrae chinensis (Turcz.) Baill. (Schisandraceae) Fructus, possesses diverse pharmacological activities including antitumor, anti-inflammation, and hepatoprotection.To explore the effect of Sch B on activated HSCs senescence in hepatic fibrosis and the mechanisms implicated.ICR mice with CCl4-induced hepatic fibrosis were supplemented with Sch B (40 mg/kg) for 30 d and LX2 cells were treated with Sch B (5, 10 and 20 μM) for 24 h. Cellular senescence was assessed by senescence-related indicators senescence-associated β-galactosidase (SA-β-gal) activity and the expression of p16, p21, p53, γ-H2AX, H3K9me3, TERT, TRF1, and TRF2. Ferric ammonium citrate (FAC) and NCOA4 siRNA were used to evaluate the mechanisms underlying Sch B's regulation of cellular senescence.Sch B (40 mg/kg) reduced serum levels of AST and ALT (53.2% and 63.6%), alleviated hepatic collagen deposition, and promoted activated HSCs senescence in mice. Treatment with Sch B (20 μM) decreased cell viability to 80.38 ± 4.87% and elevated SA-β-gal activity, with the levels of p16, p21 and p53 increased by 4.5-, 2.9-, and 3.5-fold and the levels of TERT, TRF1 and TRF2 decreased by 2.4-, 2.7-, and 2.6-fold in LX2 cells. FAC (400 μM) enhanced Sch B's effect mentioned above. NCOA4 siRNA weakened the effects of Sch B on iron deposition and HSCs senescence.Sch B could ameliorate hepatic fibrosis through the promotion of activated HSCs senescence, which might be attributed to its induction of NCOA4-mediated ferritinophagy and subsequent iron overload.