Hepatoprotective Role of Emodin in Chemical-Induced Liver Injury histopathological study in Mice Model

Abstract

Abstract Background: Carbon tetrachloride (CCl4)-induced chronic liver injury results in liver fibrosis and eventually causes cirrhosis and hepatocellular carcinoma. The current study is aimed at analyzing the impact of emodin on liver fibrosis and the inflammation in CCl4-induced liver injury among mice and the mechanisms associated with it. Objectives: The aim of the current study is to evaluate the morphological changes and the molecular mechanisms that are involved in liver fibrosis, induced by the administration of CCl4 and the potentials of emodin in treating the disease. Methods: For this study, a total of 30 male albino rats was considered and was segregated into three groups with each group containing 10 mice. The mice were treated with CCl4 for about 4-5 weeks while in parallel, emodin was administered upon the study group in the last two weeks. Then, the liver tissues were harvested from the mice to conduct morphological, biochemical and molecular analyses. Results: The outcomes obtained from hematoxylin and eosin staining followed by enzyme level analysis found that CCl4 treatment severely damaged the liver tissues of the study group mice and also incremented the liver functional enzymes. But, when the groups were treated with Emodin, the enzyme levels got reduced. This establishes the potential therapeutic effect of Emodin upon liver function. As per the molecular analysis results, CCl4 treatment increases the mRNA expression of SMAD4, α-SMA, TGF, MDA, Nrf2, and pro-inflammatory markers IL-6 and TNF-α. However, these genes got downregulated when Emodin is used along with CCl4. In addition to these, the combination also upregulated the anti-inflammatory markers such as IL-1β and IL-10, Hepatic and Cancer-specific markers HNF-α, Albumin, p53, and AFP. As per the study outcomes, it can be concluded that Emodin is a promising therapeutic agent that can be used in the treatment of liver damage and inflammation, triggered by CCl4 treatment. Conclusion: The study concludes that through the regulation of TGFβ/Smad4 pathway, Emodin attenuates the liver fibrosis and inflammation in CCl4-induced hepatic injury in mice. The results achieved establish emodion as a potential therapeutic candidate to treat liver fibrosis and inflammation.