Hepatoprotective role of emodin in chemical-induced liver injury histopathological study in mice model

Abstract

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.