Mechanism of Action of Carthamus tinctorius L.Extract on Alcoholic Liver Disease Through Modulation of Nrf2/STAT3/NF-κB Signaling Pathway
Objective To investigate the effects of Carthamus tinctorius L.extract(CTLE)on the levels of oxidative stress and inflammation in mice with ethanol-induced alcoholic liver disease and its mechanism of action.Methods SPF-grade C57BL/6 male mice were randomly divided into four groups:control group,model group,low-CTLE group(50 mg·kg-1),and high-CTLE group(100 mg·kg-1).The control group was given Lieber-Decarli liquid diet,and the other groups were given Lieber-Decarli alcohol diet to construct a chronic alcoholic liver injury model in mice.Serum and liver tissues of mice were collected and serum biochemical indexes of mice were detected.HE and oil red O staining were applied to observe pathological changes in mouse liver tissues.Real-time fluorescence quantitative PCR and Western Blot were used to detect the mRNA and protein expression levels of Keap1/Nrf2 and STAT3/NF-κB pathway-related factors.Results Compared with the model group,the ALT,AST,LDL-C,and MDA levels were significantly reduced(P＜0.05,P＜0.01),while the levels of HDL-C,SOD,and GSH were increased dramatically in the administered group(P＜0.05,P＜0.01),which indicated that CTLE has specific protective and antioxidant effects on alcoholic liver injury in mice.HE staining and oil red O staining showed that the hepatic lesions and lipid deposition of mice were ameliorated.It enhances the antioxidant and anti-inflammatory effects of the body by activating the mRNA and protein expression levels of antioxidant factors related to the Keap1/Nrf2 pathway and inhibiting the mRNA and protein expression levels of inflammatory factors related to STAT3/NF-κB pathway(P＜0.05,P＜0.01).Conclusion It was shown that CTLE could exert anti-oxidative stress and anti-inflammatory effects through regulating Keap1/Nrf2 and STAT3/NF-κB signaling pathways to attenuate alcoholic liver injury in mice.This study may provide a new idea for the treatment of alcoholic liver disease and the subsequent study of molecular mechanisms.
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