Abstract: This study aimed to investigate the protective effect of chlorogenic acid (CGA) against carbon tetrachloride (CCl4)-induced liver injury in red crucian carp and to preliminarily elucidate its mechanism based on the Nrf2/HO-1 signaling pathway. Red crucian carp were randomly divided into a control group, a model group (treated with CCl4), CGA groups at different concentrations, and a positive control group treated with silymarin. A liver injury model was established by intraperitoneal injection of CCl4. Serum activities of ALT, AST, AKP, and γ-GT, content of TG, TC, TBIL, as well as MDA content and SOD and GSH-Px activities in hepatopancreatic tissue were measured. Pathological changes in hepatopancreatic tissue were observed by HE staining. The mRNA expression levels of NFE2L2, HO-1, NQO1, and GCL in liver tissue were detected by RT-qPCR. The results showed that compared with the control group, the model group exhibited significantly increased serum levels of ALT, AST, AKP, γ-GT, and TBIL (P<0.05, P<0.01), significantly decreased activities of SOD and GSH-Px in liver tissue, and a significant increase in MDA content (P<0.05). Pathological damages such as vacuolar degeneration, pyknosis, and lysis of hepatopancreatic cells were observed. After CGA intervention, the medium- and high-dose groups showed significant improvements in serum biochemical indicators, a marked reduction in MDA content in hepatopancreatic tissue (P<0.05, P<0.01), and a significant recovery of SOD and GSH-Px activities (P<0.05), along with alleviated pathological damage in liver tissue. The silymarin group also exhibited ameliorative effects. Furthermore, the medium- and high-dose CGA groups exhibited a significant increase in the mRNA expression levels of NFE2L2, HO-1, NQO1, and GCL (P<0.05). These findings suggest that CGA alleviates CCl4-induced liver injury in red crucian carp, likely by activating the Nrf2/HO-1 signaling pathway, boosting antioxidant defenses, and reducing oxidative stress.
Keywords: red crucian carp; chlorogenic acid; liver injury; oxidative stress; Nrf2/HO-1 signaling pathway
（Acta Laser Biology Sinica, 2026, 35(3): 253-261）