Abstract

S-allyl-L-cysteine (SAC) is an organosulfur compound derived from aged garlic extract (AGE). Studies have reported that AGE possesses bioprotective capacity, including antidiabetic, antimicrobial, antioxidant, and antitumor effects. The present study examined the protective effects of SAC against carbon tetrachloride (CCl4) induced hepatotoxicity in rats. Ten male Wistar rats aged 11 - 12 weeks were randomly divided into two groups (five rats/group) as control and SAC groups. All rats had ad libitum access to water, and the SAC group received water containing SAC intragastrically (200 mg/kg) once daily for five consecutive weeks. In the fifth experimental week, 50% CCl4 in olive oil (1 mL/kg) was administered intraperitoneally three times a week to induce liver injury in both groups. Rats were sacrificed at 24 hours after the last CCl4 injection, and liver tissues were excised for histopathological, immunohistochemical and antioxidant analyses. The rats in the SAC group did not show abnormal behavior, such as decreased water intake or food consumption, during the experimental period. Body weights in all groups did not change significantly over the experimental period. Histopathological analysis showed that the percentage of hepatic steatosis was lower in the SAC group at 12.75% ± 3.74% compared to 24.64% ± 5.29% in the control group (p p 4-induced liver damage by decreasing hepatic steatosis and reducing CYP2E1 expression in rats.

Highlights

  • Oxidative damages to hepatic cells are common sequelae of many liver diseases, including hepatic steatosis, chronic hepatitis, cholestasis, and liver cirrhosis [1]

  • Histopathological analysis showed that the percentage of hepatic steatosis was lower in the SAC group at 12.75% ± 3.74% compared to 24.64% ± 5.29% in the control group (p < 0.05)

  • These results suggest that SAC can alleviate CCl4-induced liver damage by decreasing hepatic steatosis and reducing cytochrome P4502E1 (CYP2E1) expression in rats

Read more

Summary

Introduction

Oxidative damages to hepatic cells are common sequelae of many liver diseases, including hepatic steatosis, chronic hepatitis, cholestasis, and liver cirrhosis [1]. Its toxicity requires bioactivation to produce reactive metabolic intermediates using a trichloromethyl radical like CCl3 or peroxy trichloromethyl radicals ( CCl3OO ) by mixed function oxidase cytochrome P450 (CYP450) in hepatic microsomes [6]. These free radicals can bind to polyunsaturated fatty acids (PUFAs) and form alkoxy ( R ) and peroxy radicals ( ROO ), which serially generate lipid peroxide, damage cell membranes, and disrupt antioxidant enzyme activity and antioxidative substrate content, resulting in hepatic injury [7]. Mechanisms for preventing hepatotoxicity induced by oxidative stress involve blocking the chain reaction of oxidation, improving phase II antioxidant enzyme activity, and increasing levels of antioxidant substances

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call