Study on the Mechanism of Rabdosia serra in the Treatment of Alcoholic Liver Injury Based on Network Pharmacology

Objective: To investigate the protective effect and potential mechanism of Rabdosia serra on alcoholic liver injury. Method: Forty female Kunming mice were randomly divided into blank group, model group, Rabdosia serra group and positive control group. All mice received 0.1 mL/10 g white spirit to established alcoholic liver injury model, and continuous administration for 10 days. After the last administration, HE staining was used to observe the pathological changes of liver tissue. Serum indexes were determined by kit method. Network pharmacology method was used to analyze the potential effective components, signal pathways and molecular targets of Rabdosia serra in the treatment of alcoholic liver injury, and Western blot was used to verify the related molecular targets. Results: The protein expression levels of AST, m-AST and GDH in Rabdosia serra group were significantly higher than those in model group (P<0.05 or P<0.01). The protein expression levels of ADH and CAT in Rabdosia serra group were significantly higher than those in model group (P<0.05 or P<0.01). The expression levels of SOD, GSH PX and GSH protein in Rabdosia serra group were significantly higher than those in model group (P<0.05 or P<0.01), and the expression level of MDA protein in the Rabdosia serra group was significantly lower than that in the model group (P<0.05). Network pharmacological analysis showed that caffeic acid, rosmarinic acid, quercetin, cannabinoid and isorhamnetin were the most likely active substances, and Nrf2, CYP2E1, PTGS2, MMP9 and MMP2 were the most likely therapeutic targets. Western bolt results showed that compared with the model group, the expression of Nrf2 protein in Rabdosia serra group was significantly up-regulated (P<0.01), and the expression of CYP2E1 protein was significantly down regulated (P<0.01). Conclusions: Rabdosia serra had protective effect on alcoholic liver injury, and the mechanism would be related to the decrease of CYP2E1 level, activation of Nrf2 expression, and reduction of oxidative stress damage.