Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology · 2025
Cinnamaldehyde attenuates CCL4-induced liver fibrosis by inhibiting the CYP2A6/Notch3 pathway.
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Gao Sicheng, Zhang Wanyi, Gao Xiaodi, Ye Baiyang, Hu Weiye, Yang Hailin, Chai Haisheng, Yang Jiangling, Tang Qinlin, Zhao Gang, Zhu Junfeng
Аннотация
BACKGROUND: Hepatic stellate cells (HSCs) activation and hepatocyte injury contribute to liver fibrosis progression and subsequent cirrhosis. Literature showed that cinnamaldehyde (CA) could alleviate fibrosis procession and steatosis. However, its specific role in liver fibrosis remains largely unexplored.
MATERIALS AND METHODS: Liver fibrosis was induced in vivo, and CA was administered for 4 weeks. Liver inflammation, fibrosis, apoptosis, and proliferation were evaluated using histological, western blotting, and immunohistochemistry. CYP2A6 and Notch3 expression levels were also measured. In vitro, TGF-β stimulated LX2 cell activation was used, and siCYP2A6 was employed to evaluate the anti-fibrosis mechanism of CA.
RESULTS: CA effectively improved liver function and reduced fibrosis in CCL4-treated rats, significantly decreasing serum ALT, AST, GGT, TBIL, and HAase levels (all p < 0.05), with a notable increase in ALB in the high-dose group. Histologically, CA reduced hepatic disorganization and collagen proliferation, significantly diminishing fibrotic areas in the CA-H group (p < 0.05). CA also downregulated α-SMA and collagen I expression, and suppressed TGF-β activity. In TGF-β1-stimulated LX2 cells, CA treatment led to significant reductions in CYP2A6 and Notch3 expression (p < 0.05), highlighting its regulatory effects on key fibrotic pathways.
CONCLUSIONS: CA alleviated CCL4-induced liver fibrosis with inhibition of HSCs activation and liver inflammation and reduced hepatocyte apoptosis, potentially linked to the HSCs-mediated CYP2A6/Notch3 modulation.
MATERIALS AND METHODS: Liver fibrosis was induced in vivo, and CA was administered for 4 weeks. Liver inflammation, fibrosis, apoptosis, and proliferation were evaluated using histological, western blotting, and immunohistochemistry. CYP2A6 and Notch3 expression levels were also measured. In vitro, TGF-β stimulated LX2 cell activation was used, and siCYP2A6 was employed to evaluate the anti-fibrosis mechanism of CA.
RESULTS: CA effectively improved liver function and reduced fibrosis in CCL4-treated rats, significantly decreasing serum ALT, AST, GGT, TBIL, and HAase levels (all p < 0.05), with a notable increase in ALB in the high-dose group. Histologically, CA reduced hepatic disorganization and collagen proliferation, significantly diminishing fibrotic areas in the CA-H group (p < 0.05). CA also downregulated α-SMA and collagen I expression, and suppressed TGF-β activity. In TGF-β1-stimulated LX2 cells, CA treatment led to significant reductions in CYP2A6 and Notch3 expression (p < 0.05), highlighting its regulatory effects on key fibrotic pathways.
CONCLUSIONS: CA alleviated CCL4-induced liver fibrosis with inhibition of HSCs activation and liver inflammation and reduced hepatocyte apoptosis, potentially linked to the HSCs-mediated CYP2A6/Notch3 modulation.