By: Yanfei Wang, Xiangda Meng, Shimin Wang, Hongting Sui, Wenjuan Wang, Guohua Li, Liping Cong, Chao Wu, Ting Cao, Jing Zhang
Keywords: Carcinogenesis of cirrhosis; Hepatic stellate cells; Icariin; miR-145; ROS-NLRP3 pathway
DOI : 10.36721/PJPS.2026.39.4.REG.15414.1
Abstract: Background: Hepatocarcinogenesis arising from liver cirrhosis is a major contributor to hepatocellular carcinoma (HCC), but effective interventions remain limited Objective: This study aimed to elucidate the molecular mechanism by which icariin suppresses cirrhosis-to-cancer progression through the ROS/NLRP3/miR-145 axis. Methods: Fifty Sprague-Dawley rats were randomly assigned to five groups: control, model, low-dose icariin (ICA-L), high-dose icariin (ICA-H), and positive control. In vitro, SMMC-7721 and HepG2 cells were treated with TGF-?1 and various concentrations of icariin to assess their effects on hepatocellular carcinoma cell activity. Results: Compared with the model group, icariin significantly reduced the liver index, serum AFP levels, Ki-67 positivity, and hepatic ROS levels in rats, suppressed NLRP3 expression, upregulated miR-145, and effectively ameliorated liver fibrosis and dysplasia (P<0.05). In SMMC-7721 cells, icariin inhibited TGF-?1-induced proliferation, migration and invasion, promoted apoptosis and G0/G1 phase arrest, while concurrently increasing exosomal miR-145 levels (P<0.05). Further mechanism verification confirmed that miR-145 directly targets and inhibits NLRP3 expression. Conclusion: Icariin effectively inhibits cirrhosis-associated carcinogenesis by suppressing the ROS-NLRP3 pathway and upregulating miR-145, providing a theoretical basis for the prevention and treatment of cirrhosis and hepatocellular carcinoma.
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