Canadian journal of gastroenterology & hepatology · 2025
Rabdosia rubescens Inhibits CYP7A1 Expression and Induces Autophagy to Reduce Alcohol-Induced Liver Damage in Mice.
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Zou Xi, Chen Wei, Shao Yidan, Shi Tingting, Ke Yunling
Аннотация
OBJECTIVE: Investigating the antialcoholic liver injury properties of Rabdosia rubescens and its effect on the expression of CYP7A1 and levels of autophagy.
MATERIALS AND METHODS: Male C57BL/6 mice were randomly divided into three groups, namely, the control group (Lieber-DeCarli standard diet), model group (Lieber-DeCarli ethanol diet), and treatment group (Rabdosia rubescens at concentrations of 50 mg/kg, 100 mg/kg, and 200 mg/kg). The mice were fed their respective diets for 10 days, with the treatment group receiving the corresponding concentration of Rabdosia rubescens. On the 11th day, all the mice except those in the control group were given 30% EtOH. Nine hours later, the mice were sacrificed and their blood serum and liver tissue were collected for analysis. The effect of Rabdosia rubescens on alcohol-induced liver damage was evaluated by testing serum biochemical indicators, liver bile acid content, liver tissue histopathological changes, liver LC3 and p62 immunohistochemical staining, liver inflammatory factors, and CYP7A1, SREBP, FAS, LC3, Beclin-1, ATG7, and p62 expressions.
RESULTS: Compared with the model group, Rabdosia rubescens was found to significantly reduce the levels of ALT, AST, TG, TC, and TBA in the serum of mice with alcoholic liver injury (p < 0.05 or p < 0.01). Rabdosia rubescens was found to significantly reduce the level of apoptosis in H&E-stained liver tissue sections. Rabdosia rubescens also significantly reduced the levels of TNF-α and IL-1β in the livers of mice (p < 0.001). Rabdosia rubescens was found to induce the expression of LC3, Beclin-1, and ATG7 proteins and mRNA, while inhibiting the expression of CYP7A1, SREBP, FAS, and p62 proteins and mRNA (p < 0.05 or p < 0.01).
CONCLUSION: Rabdosia rubescens has been shown to relieve alcohol-induced liver damage in mice by reducing levels of CYP7A1, alleviating cholestasis and reducing inflammation. It can also reduce alcohol-induced liver damage by decreasing fat synthesis and inducing autophagy.
MATERIALS AND METHODS: Male C57BL/6 mice were randomly divided into three groups, namely, the control group (Lieber-DeCarli standard diet), model group (Lieber-DeCarli ethanol diet), and treatment group (Rabdosia rubescens at concentrations of 50 mg/kg, 100 mg/kg, and 200 mg/kg). The mice were fed their respective diets for 10 days, with the treatment group receiving the corresponding concentration of Rabdosia rubescens. On the 11th day, all the mice except those in the control group were given 30% EtOH. Nine hours later, the mice were sacrificed and their blood serum and liver tissue were collected for analysis. The effect of Rabdosia rubescens on alcohol-induced liver damage was evaluated by testing serum biochemical indicators, liver bile acid content, liver tissue histopathological changes, liver LC3 and p62 immunohistochemical staining, liver inflammatory factors, and CYP7A1, SREBP, FAS, LC3, Beclin-1, ATG7, and p62 expressions.
RESULTS: Compared with the model group, Rabdosia rubescens was found to significantly reduce the levels of ALT, AST, TG, TC, and TBA in the serum of mice with alcoholic liver injury (p < 0.05 or p < 0.01). Rabdosia rubescens was found to significantly reduce the level of apoptosis in H&E-stained liver tissue sections. Rabdosia rubescens also significantly reduced the levels of TNF-α and IL-1β in the livers of mice (p < 0.001). Rabdosia rubescens was found to induce the expression of LC3, Beclin-1, and ATG7 proteins and mRNA, while inhibiting the expression of CYP7A1, SREBP, FAS, and p62 proteins and mRNA (p < 0.05 or p < 0.01).
CONCLUSION: Rabdosia rubescens has been shown to relieve alcohol-induced liver damage in mice by reducing levels of CYP7A1, alleviating cholestasis and reducing inflammation. It can also reduce alcohol-induced liver damage by decreasing fat synthesis and inducing autophagy.