Potential Hepatoprotective Effects of Allicin on Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Oxidative Stress, Inflammation, and Apoptosis

• DOI: 10.3390/toxics12050328
• Publication Date: 2024-04-30T12:14:31Z
• Authors: Qianmei Gong; Xiaoming Wang; Yongshi Liu; Heling Yuan; Zifeng Ge; Yuzhou Li; Jinhu Huang; Yufan Liu; Ming Chen; Wenjun Xiao; Ruiting Liu; Rongmei Shi; Liping Wang
• Keywords: 0301 basic medicine; 03 medical and health sciences; proinflammatory cytokine; Chemical technology; allicin; TP1-1185; acute liver injury; anti-inflammation; Nrf2; Article

The global burden of liver disease is enormous, which highlights the need for effective hepatoprotective agents. It was reported that allicin exhibits protective effects against a range diseases. In this study, we further evaluated allicin’s effect and mechanism in acute hepatic injury. Liver injury mice induced by intraperitoneal injection with 1% CCl4 (10 mL/kg/day). When first dose given, given immediately after administration different doses (40, 20, 10 mg/kg/day) as well compound glycyrrhizin (CGI, 80 mg/kg/day), then were administrated every 12 h. animals dissected 24 h administration. findings demonstrated significant inhibition CCl4-induced following treatment. This evidenced notable reductions serum levels transaminases, specifically aspartate transaminase, along mitigated histological damage to liver. process, plays role reducing amounts or expression proinflammatory cytokines, IL-1β, IL-6. Furthermore, recovered activities antioxidant enzyme catalase (CAT) reduced production malondialdehyde (MDA) dose-dependent manner, also Caspase 3, 8, BAX inhibit cell apoptosis. Further analysis showed inhibited increased protein Nuclear factor-erythroid 2-related factor 2 (Nrf2) NAD(P)H:quinone oxidoreductase 1 (NQO1), related inflammation oxidative stress. vitro study LPS-induced RAW264.7 inflammatory model confirmed can important inflammation-related factors alleviate inflammation. research firstly clarified has on via inhibiting response hepatocyte apoptosis, alleviating stress associated progress damage, highlighting potential agent.