Liver diseases caused by viral infections, alcoholism, drugs, or chemical poisons are a significant health problem: Liver diseases are a leading contributor to mortality, with approximately 2 million deaths per year worldwide. Liver fibrosis, as a common liver disease characterized by excessive collagen deposition, is associated with high morbidity and mortality, and there is no effective treatment. Numerous studies have shown that the accumulation of mast cells (MCs) in the liver is closely associated with liver injury caused by a variety of factors. This study investigated the relationship between MCs and carbon tetrachloride (CCl4)-induced liver fibrosis in rats and the effects of the MC stabilizers sodium cromoglycate (SGC) and ketotifen (KET) on CCl4-induced liver fibrosis. The results showed that MCs were recruited or activated during CCl4-induced liver fibrosis. Coadministration of SCG or KET alleviated the liver fibrosis by decreasing SCF/c-kit expression, inhibiting the TGF-β1/Smad2/3 pathway, depressing the HIF-1a/VEGF pathway, activating Nrf2/HO-1 pathway, and increasing the hepatic levels of GSH, GSH-Px, and GR, thereby reducing hepatic oxidative stress. Collectively, recruitment or activation of MCs is linked to liver fibrosis and the stabilization of MCs may provide a new approach to the prevention of liver fibrosis.

中文翻译：

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肝脏中肥大细胞的募集或激活加剧了四氯化碳引起的肝损伤中纤维化的积累

由病毒感染、酗酒、药物或化学毒物引起的肝病是一个严重的健康问题：肝病是导致死亡的主要原因，全世界每年约有 200 万人死亡。肝纤维化是一种以胶原过度沉积为特征的常见肝脏疾病，其发病率和死亡率较高，且尚无有效的治疗方法。大量研究表明，肝脏中肥大细胞（MCs）的积累与多种因素引起的肝损伤密切相关。本研究探讨了MCs与四氯化碳（CCl4）诱导的大鼠肝纤维化之间的关系以及MC稳定剂色甘酸钠（SGC）和酮替芬（KET）对CCl4诱导的肝纤维化的影响。结果表明，MCs 在 CCl4 诱导的肝纤维化过程中被招募或激活。 SCG或KET联合用药通过降低SCF/c-kit表达、抑制TGF-β1/Smad2/3通路、抑制HIF-1a/VEGF通路、激活Nrf2/HO-1通路、增加肝纤维化来减轻肝纤维化。 GSH、GSH-Px 和 GR 水平，从而减少肝脏氧化应激。总的来说，MCs 的募集或激活与肝纤维化有关，MCs 的稳定可能为预防肝纤维化提供新方法。