四氯化碳
四氯化碳
番茄红素
内科学
氧化应激
内分泌学
纤维化
肝纤维化
抗氧化剂
炎症
化学
医学
自噬
脂肪变性
细胞凋亡
生物化学
有机化学
作者
Wei Li,Yuxin Jiang,Ting-Ting Yu,Hao Wu,Guoguang Wang
标识
DOI:10.3325/cmj.2023.64.243
摘要
AimTo evaluate the effect of lycopene on carbon tetrachloride (CCl4)-induced hepatic fibrosis and elucidate the underlying mechanism.MethodsMale rats were randomly assigned to the control group, CCl4 group, and lycopene group. The CCl4 group was intraperitoneally injected with CCl4 twice per week for 12 weeks to induce hepatic fibrosis. The control group was intraperitoneally injected with olive oil. Lycopene was orally administered during CCl4 treatment. Body weight and liver weight were recorded. Liver function was assessed. Biomarkers of oxidative stress and inflammatory factors were measured. Histological changes and collagen expression were evaluated. The expression of TGF-β1, α-SMA, HO-1, SIRT 1, REDD1, SHP2, P62, and LC3 in the liver was determined, as well as the levels of phosphorylated NF-κB and IκB α.ResultsLycopene significantly reduced the liver/body weight ratio, and AST (P = 0.001) and ALT levels (P = 0.009). It also significantly increased CAT and SOD activities (P < 0.001) and decreased MDA content (P < 0.001), IL-6 (P < 0.001), and TNF-α (P = 0.001). Histological analysis demonstrated that lycopene improved lobular architecture and decreased collagen expression. It also decreased the expression of TGF-β1, α-SMA, P62, and SHP2, and increased the ratio of LC3 II/I, as well as Beclin 1 and REDD1 expression. In addition, it reduced NF-κB and IκB-α phosphorylation, and elevated the levels of HO-1, SIRT 1, and PGC 1α.ConclusionLycopene attenuates CCl4-induced hepatic fibrosis because of its effect on autophagy by reducing oxidative stress and inflammation.
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