Objective To study the effect and mechanism of invigorating spleen, clearing heat and eliminating stasis drugs on QOUH of gastric mucosa and expression of EGF and EGFR in rat model of gastric ulcer. Methods The rat model of gastric ulcer was constructed by injection of acetic acid. The rats were randomly divided into model group, ranitidine group, invigorating spleen group, clearing heat group, eliminating stasis group, complex prescription group and normal control group. The ulcer index (UI), regenerate mucosal thickness, lamina muscularis mucosal width were observed by HE, and the level of EGF was detected by ELISA. The expression of EGFR in the mucosa around the ulcer was detected by SABC kit immunohistochemical method. Results Compared with model group, the regenerate mucosal thickness, lamina muscularis mucosae defect width and UI in invigoraing spleen, clearing heat, elimianting stasis and complex prescription groups were different significantly (P

Objective To develop the ribavirin purity certified reference material( CRM ) which has measurement traceability and high accuracy,and establish an effective method of evaluation. Methods The homogeneity and the stability were checked by differential scanning calorimetry(DSC). High performance liquid chromatography(HPLC)and DSC methods were used for purity determination of ribavirin. Results Ribavirin showed satisfactory homogeneity and stability. The certified value of ribavirin was 99. 5%with an uncertainty of 0. 4%(k=2,P=0. 95). Conclusion Ribavirin purity CRM obtained in this paper has been proven to be a national primary CRM with high accuracy and traceability,which can be used to validate analytical methods,improve the accuracy of measurement data,establish meteorological traceability of analytical results as well as control the quality of ribavirin in the pharmaceutical industry.

The purpose of this study was to investigate the effects of salvianolic acid A (SAA) in systemic lupus erythematosus (SLE) induced by pristane in BALB/c mice. Lupus mice were established by confirming elevated levels of autoantibodies and IL-6 after intraperitoneal injection of pristane. Mice were then treated with daily oral doses of SAA for 5 months in parallel with mice treated with prednisone and aspirin as positive controls. The levels of autoantibodies were monitored at monthly intervals and nephritic symptoms observed by hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining. Western blot analysis of renal tissue was also employed. SAA treatment caused a significant reduction in the levels of anti-Sm autoantibodies and reduced renal histopathological changes and pathological effects. SAA treatment also significantly inhibited the phosphorylation of IKK, IB and NFB in renal tissues of lupus mice. In conclusion, the results suggest that SAA alleviates renal injury in pristane-induced SLE in BALB/c mice through inhibition of phosphorylation of IKK, IB and NFB.