ABSTRACT
AIM To study the effects of dexamethasone on expressing monocyte chemoattractant protein-1(MCP-1 ) mRNA in the rats with pulmonary fibrosis, elaborate the molecular mechanism of dexamethasone (Dxs) in pulmonary fibrosis therapy. METHODS The model of pulmonary fibrosis was established by instilling bleomycin intratracheally. After treating with Dxsip, the levels of MCP-1 mRNA were determined by RT-PCR. The histological changes were observed and the numbers of inflammatory cells were counted in optical microscopy field. RESULTS The accumulation of inflammatory cells decreased markedly, and the symptom of pulmonary fibrosis was alleviated. Furthermore, Dxs evidently inhibited the expression of MCP-1 mRNA in lung tissues with pulmonary fibrosis. CONCLUSION The molecular mechanism of Dxs in pulmonary fibrosis therapy was associated with inhibiting the expression of MCP-1 mRNA.
ABSTRACT
The LVdP/dtmax, LVSP, AP and Vmax of the rat hearts in vivo were increased by Sophoridine ( 2 mg/kg, given to rats iv ) by 19.5, 13.1, 14.8 and 28.2% respectively. Such a positive inotropic effect lasted for more than 5 min and was statistically significant. Adrenaline (0.16 ?g/kg, iv ) could also increase the LVdP/dtmax and Vmax of the heart obviously and this action was not stronger than Sri after uses of drugs except at 0.5 min and vanished more quickly. There was an increment of MVO2I because of the increased arterial pressure within 3 min after use of Sri, which was much less than adrenaline. The present results show Sri strengthened the cardial force for longer time and affected the arterial pressure and MVO2I less than adrenaline in the rat hearts in vivo.
ABSTRACT
AIM To study the effects of dexamethasone on expressing monocyte chemoattractant protein 1(MCP 1 ) mRNA in the rats with pulmonary fibrosis, elaborate the molecular mechanism of dexamethasone (Dxs) in pulmonary fibrosis therapy. METHODS The model of pulmonary fibrosis was established by instilling bleomycin intratracheally. After treating with Dxs ip , the levels of MCP 1 mRNA were determined by RT PCR. The histological changes were observed and the numbers of inflammatory cells were counted in optical microscopy field. RESULTS The accumulation of inflammatory cells decreased markedly, and the symptom of pulmonary fibrosis was alleviated. Furthermore, Dxs evidently inhibited the expression of MCP 1 mRNA in lung tissues with pulmonary fibrosis. CONCLUSION The molecular mechanism of Dxs in pulmonary fibrosis therapy was associated with inhibiting the expression of MCP 1 mRNA.