Role of Vitamin D Supplementation with Liv-52 on Inflammatory Biomarkers in Carbon Tetrachloride (Ccl4) Induced Liver Disease in Wister Rats

Abstract

Introduction: Liver disease is a significant global health concern, with a wide range of etiologies and adverse effects on overall health. Among the various causes of liver disease, exposure to hepatotoxins such as carbon tetrachloride (CCl4) has been widely studied. Inflammatory processes play a crucial role in the development and progression of liver disease. Inflammatory biomarkers, serve as important indicators of liver injury and can provide insights into the underlying inflammatory response. Therefore, identifying effective interventions that can modulate these inflammatory biomarkers holds great promise for the management of liver disease. The goal of the current study was to examine the anti-inflammatory effects of vitamin D combined with Liv-52 on liver disease caused by CCl4. Materials and Methods: Male Wistar rats were given CCl4, twice a week for nine weeks, Liv-52 (1 mL/kg b.w), and vitamin D (500 IU/kg b.w) orally for nine weeks. The effects of vitamin D supplementation along with Liv-52 on inflammatory markers were estimated in the serum samples. Results: When compared to control animals, it was discovered that the hepatotoxic carrying animals had higher serum concentrations of IL-6, TGF-β and TNF-α. Supplementation of vitamin D (group III) and Liv-52 (group IV) treated rats showed significantly reduced the levels of IL-6, TGF-β and TNF-α when compared with group II animals. The supplementation with combination of vitamin D and liv-52 more significantly reduced the levels of IL-6, TGF-β and TNF-α. The comparative analysis between group III vs IV, the protective function of vitamin D in-isolation is similar to the protection by Liv-52 in-isolation, there is no marker difference between the two and both have significant protection effect. Conclusion: The results obtained indicate that the combination of vitamin D supplementation and Liv-52 exhibited beneficial effects on inflammatory biomarkers in CCl4-induced liver disease.