Original scientific paper
https://doi.org/10.3325/cmj.2023.64.243
Lycopene improves autophagy and attenuates carbon tetrachloride-induced hepatic fibrosis in rats
Wei Li
; Department of Pathophysiology, Wannan Medical College, Wuhu, China
Yuxin Jiang
; Jiaxing University, Jiaxing, China
Wei Hao
; Experimental Center for Function Subjects, Wannan Medical College, Wuhu, China
Guoguang Wang
; Department of Pathophysiology, Wannan Medical College, Wuhu, China
*
* Corresponding author.
Abstract
Aim To evaluate the effect of lycopene on carbon tetrachloride (CCl4
)-induced hepatic fibrosis and elucidate the
underlying mechanism.
Methods Male 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.
Results Lycopene 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.
Conclusion Lycopene attenuates CCl4
-induced hepatic fibrosis because of its effect on autophagy by reducing oxidative stress and inflammation.
Keywords
Hrčak ID:
331839
URI
Publication date:
31.8.2023.
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