The Effect of Berberine on Thioacetamide Induced Hepatic Toxicity in Rats

Eldeeb, Maha; Tahoon, Nahid; Abdalfattah, Ahmed Alsayed; Younis, Reham Lotfy

doi:10.21608/besps.2023.222916.1147

The Effect of Berberine on Thioacetamide Induced Hepatic Toxicity in Rats

Document Type : Original Article

Authors

Medical Physiology Department, Faculty of Medicine, Tanta University, Tanta, Egypt

10.21608/besps.2023.222916.1147

Abstract

Background: Most hepatotoxic chemicals primarily harm the liver by lipid peroxidation and oxidative damages.
Aim: To study the impact of Berberine on thioacetamide-induced hepatic toxicity and its underlying mechanisms.
Methods: This work was performed on 40 male albino rats. The animals were randomly divided into 4 groups (10 rats each): Control group: was given 0.5 ml saline intraperitoneal injection (IP) twice /week for 8 weeks. Berberine group: was given Berberine (200 mg/kg/day) by oral gavage plus 0.5 ml saline by IP twice /week for 8 weeks. Thioacetamide group: received 200mg/kg thioacetamide I.P. twice /week for 8 weeks. berberine treated group: was given 200mg/kg thioacetamide I.P. twice /week plus Berberine 200 mg/kg/day by oral gavage for 8 weeks.
Results: Berberine group showed insignificant change in all studied parameters as compared to control group. While thioacetamide group demonstrated significant elevation in serum level of bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), interleukin 6 and hepatic hydroxyproline, with significant decrease in serum level of total antioxidant capacity compared to control and berberine group. However, thioacetamide group treated with Berberine 200 mg showed significant decrease in serum level of AST, ALT, ALP, bilirubin, interleukin 6 and hepatic hydroxyproline, with significant elevation in serum level of total antioxidant capacity as compared to liver toxicity group.

Conclusions: BBR may be considered a therapeutic agent against hepatic injury, its hepatoprotective mechanism might be mediated via suppression of inflammation, oxidative stress, endogenous antioxidant defense system activation and reduction of DNA damage.

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