Chronic liver injury caused by carbon tetrachloride (CCl4) induces liver fibrosis, which can escalate to cirrhosis and hepatocellular carcinoma. This study investigated emodin’s impact on CCl4-induced liver fibrosis and inflammation in mice, along with its underlying mechanisms. While previous studies have acknowledged CCl4's role in liver fibrosis, the potential therapeutic value of emodin remains inadequately explored. The study sought to bridge this gap by assessing morphological changes and molecular mechanisms contributing to CCl4-induced liver fibrosis and investigating emodin's potential therapeutic effects. Thirty male albino rats were split into three groups (n = 10 each), undergoing an 8-week CCl4 regimen, supplemented by emodin during the final 2 weeks. Morphological, biochemical, and molecular analyses were performed on liver tissues. Hematoxylin and eosin staining, as well as enzyme-level assessments, exposed significant liver damage and elevated liver enzyme levels due to CCl4 exposure. In contrast, emodin administration resulted in reduced enzyme levels, indicating potential therapeutic benefits for liver function. Molecular analysis revealed increased mRNA expression of markers like SMAD4, α-SMA, TGF, MDA, Nrf2, and pro-inflammatory factors IL-6 and TNF-α due to CCl4. However, combined emodin and CCl4 treatment downregulated these genes and upregulated anti-inflammatory markers IL-1β and IL-10, alongside hepatic and cancer-specific markers like HNF-α, albumin, p53, and AFP. These findings suggest emodin as a therapeutic agent for mitigating CCl4-induced liver damage and inflammation. Emodin's regulation of the TGFβ/Smad4 pathway plays a pivotal role in attenuating liver fibrosis and inflammation caused by CCl4. Consequently, this study bridges the gap between animal studies and potential clinical applications, providing crucial insights for future therapeutic strategies addressing liver fibrosis and inflammation.

四氯化碳（CCl4）引起的慢性肝损伤会诱发肝纤维化，进而升级为肝硬化和肝细胞癌。本研究调查了大黄素对 CCl4 诱导的小鼠肝纤维化和炎症的影响及其潜在机制。虽然之前的研究已经承认 CCl4 在肝纤维化中的作用，但大黄素的潜在治疗价值仍未得到充分探索。该研究试图通过评估导致四氯化碳诱导的肝纤维化的形态变化和分子机制并研究大黄素的潜在治疗作用来弥补这一差距。将 30 只雄性白化大鼠分为三组（每组 10只 ），接受为期 8 周的 CCl4 治疗方案，并在最后 2 周补充大黄素。对肝组织进行形态学、生化和分子分析。苏木精和伊红染色以及酶水平评估显示，由于 CCl4 暴露，导致了严重的肝损伤和肝酶水平升高。相反，服用大黄素会导致酶水平降低，表明对肝功能具有潜在的治疗益处。分子分析显示，CCl4 导致 SMAD4、α-SMA、TGF、MDA、Nrf2 以及促炎因子 IL-6 和 TNF-α 等标志物的 mRNA 表达增加。然而，大黄素和 CCl4 联合治疗下调了这些基因，并上调了抗炎标记物 IL-1β 和 IL-10，以及肝脏和癌症特异性标记物，如 HNF-α、白蛋白、p53 和 AFP。这些发现表明大黄素可以作为减轻 CCl4 引起的肝损伤和炎症的治疗剂。大黄素对 TGFβ/Smad4 通路的调节在减轻 CCl4 引起的肝纤维化和炎症方面发挥着关键作用。因此，这项研究弥合了动物研究和潜在临床应用之间的差距，为未来解决肝纤维化和炎症的治疗策略提供了重要的见解。