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Objective: To establish a animal model of hepatic steatosis induced by chronic viral hepatitis in C(57)BL/6 mice., Methods: C(57)BL/6 mice were randomly assigned to control group, high-fat diet group, mouse hepatitis virus strain A59 (MHV-A59) virus infection group, and high-fat diet plus virus infection group. At 13 weeks of the experiment, serum samples were collected to detect MHV antibodies and transaminase and lipid levels. The hepatic pathologies of the mice were examined with Oil red O staining of the frozen sections the and HE staining of paraffin-embedded sections., Results: The mice in the two virus infection groups showed strong positivity of MHV antibodies in the serum. Compared with the control group, the mice in high-fat diet group and the two virus infection groups had significantly increased AST and ALT levels with also elevated TC and LDL-C levels. The two virus infection groups both exhibited obvious pathologies in the liver characteristic of chronic viral hepatitis with increased lipid accumulation in the hepatocytes., Conclusion: We have successfully established a mouse model of hepatic steatosis induced by chronic viral hepatitis, which provides the basis for further study of the disease mechanism.

Objective: To investigate the variation and the effect of TNF and NO in the process of the creation of protective heat stress model and provide more thoretical basis., Methods: The rats were properly treated with heat and then the serum was separated. Radioimmunoassay and nitrate reductase assay were employed to measure the concentration of TNF and NO at different time between 0 h and 24 h after heat stress respectively., Results: Compared with the control, the concentration of TNF increased significantly 2 h, 4 h, 8 h, 12 h after heat stress, of which 2 h, 12 h(P < 0.05), 4 h, 8 h(P < 0.01), but no significant changes 0 h, 24 h after heat stress. The concentration reached the peak 4 h after heat stress[(3.35 +/- 0.20) ng/ml] and increased significantly than 0 h, 2 h, 8 h, 12 h, 24 h after heat stress(P < 0.01, P < 0.05). 24 h after heat stress it recovered to normal standard. Compared with the control, the concentration of NO was higher 2 h, 4 h, 8 h, 12 h, 24 h after heat stress(P < 0.05), but no significance at 0 h. The concentration amounted to peak 8 h after heat stress[(108.21 +/- 27.89) mumol/L] and increased than 0 h, 2 h, 4 h after heat stress(P < 0.01). After 8 h it began to decrease continuously in heat stress group, however it was higher 24 h after heat stress than control., Conclusion: TNF and NO played an important role in the process of the creation of protective heat stress model.