ABSTRACT
@#This study aims to discuss the therapeutic effect of magnesium isoglycyrrhizinate on hepatitis B virus(HBV)transgenic mouse and its effect on cellular immunity and liver inflammation. The changes of serum aspartate aminotransferase(AST)and alanine aminotransferase(ALT)activity, the difference of serum hepatitis B surface antigen(HBsAg), liver tissue HBsAg mRNA, and the pathological morphological changes of liver tissue were detected to investigate the hepatic inflammatory lesions and the efficacy of magnesium isoglycyrrhizinate in HBV transgenic mouse. Peripheral blood lymphocytes were classified by flow cytometry, and serum cytokines were detected by cytometric bead array(CBA)to explore the mechanism of magnesium isoglycyrrhizinate to reduce hepatic inflammatory lesions in HBV transgenic mouse. After grouping HBV transgenic mouse with serum transaminase activity and 35 days of continuous administration, serum transaminases level in magnesium isoglycyrrhizinate ［15 mg/(kg ·d)］ group was significantly lower than that in control group(P< 0. 05), serum HBsAg protein and liver tissue HBsAg mRNA increased with time, but there was no significant difference between the two groups. The main pathological changes of liver were liver cell swelling, necrosis and focal inflammatory cell infiltration, and the pathological changes of liver in magnesium isoglycyrrhizinate group were lighter than those in control group. The number of CD8+ cells in the blood of magnesium isoglycyrrhizinate group was significantly less than that in the control group(P< 0. 05)and the CD4+/CD8+ cell ratio was significantly higher than that in the control group(P< 0. 05). The content of inflammatory cytokines in serum of magnesium isoglycyrrhizinate group decreased significantly(P< 0. 05). Magnesium isoglycyrrhizinate can regulate the immune function of HBV transgenic mouse, decrease the infiltration of inflammatory cells in hepatic tissue and hepatocyte injury, but do not affect the expression of hepatocyte HBsAg.
ABSTRACT
@#The genome, replication mode and nosogenesis of duck hepatitis B virus are similar to those of human hepatitis B virus. In addition, the natural host of duck hepatitis B virus is readily available, cheap and has a high success rate of infection. Therefore, duck hepatitis B virus-infected models have been widely used for drug screening, pharmacological and pathological studies. For drug screening, the model is easy to obtain with high infection success rate and good stability. In the pharmacological research, the model can maintain high levels of viral DNA replication in the hepatocytes and exhibit significant damaged liver phenotypes which can reflect the pharmacological effects of drugs with different mechanisms. Also in the pathologic mechanisms research, the model has entire virus life cycle and maintains a pool of covalent closed-loop DNA in the hepatocytes, which can help scientific researchers better understand human hepatitis B virus. This article reviews the applications of duck hepatitis B animal model in drug screening, pharmacological and pathological studies, also outlooks the application prospect of this model.
ABSTRACT
Objective:To investigate the effects of Origin-Preserving Decoction on the proliferation of marrow hematopoietic cells in aplastic anemia mice. Methods:Based on experimental AA models induced by Benzene and 60Co radiation in mice, the experiments including semi-solid colony culture (CFU-GM、CFU-E、BFU-E) and liquid culture (MTT Assay) were undertaken to investigate the effects of Origin-Preserving Decoction on the proliferation of marrow hematopoietic cells in AA mice. Results:Origin-Preserving Decoction (3g/kg) (ig.) could improve the outputs of CFU-GM, CFU-E and BFU-E in AA mice damaged by benzene and 60Co radiation: MTT assay showed that Origin-Preserving Decoction could stimulate the hematopoeisis of bone marrow of AA mice radiated by 60Co. Conclusions: Origin-Preserving Decoction has a good future for AA therapy.