Multi-Efficacy of One Drug (MEOD) refers to the traditional Chinese medicines (TCM) with diverse efficacies.MEOD,one of the important characteristics of TCM,is regarded as the basis of clinical rational drug use.However,there have been few reports on the MEOD research so far.In this paper,with rhubarb selected as a typical model drug,metabolomics and network pharmacology analysis are integrated to investigate the mechanisms of MEOD with the employment of the two animal models of constipation and jaundice.Then,the biological target network of MEOD is established for promoting the precision of the quality control and clinical use of TCM.

OBJECTIVE:To study the effects of high-mobility group box 1 protein(HMGB1) -mediated inflammatory pathway HMGB1-Toll like receptor 4 (TLR4) /nuclear transcription factor κ B(NF-κ B)on liver injury of rats induced by Tripterygium wilfordii,and to provide reference for clarify the mechanism of liver injury induced by T.wilfordii. METHODS:Totally 24 SD rats were randomly divided into blank group(normal saline,i. g. ),T. wilfordii group(16 g/kg by crude drug,i. g. )and neutralizer group(16 g/kg T. wilfordii crude drug i. g. after i. p injection of 100 mg/kg Ammonium glycyrrhizinate solution 3 h),with 8 rats in each group. All rats were treated for consecutive 3 weeks. The serum levels of AST and ALT in rats were detected every week. After the end of medication,the serum levels of HMGB1,IL-1β,IL-2 and TNF-α were detected by ELISA method;the protein expression of HMGB1,NF-κB p65 and TLR4 in liver tissue of rats were detected by Western blot assay. The pathological changes of liver tissue in rats were measured with HE staining method. RESULTS:After 3 weeks of treatment,the serum levels of AST, ALT,HMGB1,IL-1β,IL-2 and TNF-α in rats,the protein expression of HMGB1,NF-κB p65 and TLR4 in liver tissue of rats in T. wilfordii group were significantly higher than blank group and neutralizer group(P<0. 05 or P<0. 01). Hepatocyte edema was found around the central vein of the liver,and circular vacuoles were seen in some hepatic cytoplasm in T. wilfordii group;only varying size of vacuoles were found in a small number of cells in neutralizer group. CONCLUSIONS:T. wilfordii induced liver injury may be associated with the activation of HMGB1-TLR4/NF-κB inflammation pathway.

Although oxymatrine (OMT) has been shown to directly inhibit the replication of hepatitis B virus (HBV), limited research has been done with this drug. In the present study, the antiviral effect of OMT was investigated in an immunocompetent mouse model of chronic HBV infection. The infection was achieved by tail vein injection of a large volume of DNA solution. OMT (2.2, 6.7 and 20 mg/kg) was administered by daily intraperitoneal injection for 6 weeks. The efficacy of OMT was evaluated by the levels of HBV DNA, hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) and hepatitis B core antigen (HBcAg). The immunoregulatory activity of OMT was evaluated by serum ELISA and flow cytometry. Results shows that OMT at 20 mg/kg inhibited HBV replication, and it was more efficient than entecavir (ETV) in the elimination of serum HBsAg and intrahepatic HBcAg. In addition, OMT accelerated the production of interferon-(IFN-) in a dose-dependent manner in CD4T cells. Our findings demonstrate the beneficial effects of OMT on the enhancement of immunological function and in the control of HBV antigens. The findings suggest this drug to be a good antiviral therapeutic candidate for the treatment of HBV infection.