论文部分内容阅读
目的:研究白及多糖抗二氧化硅诱导的实验性矽肺大鼠肺纤维化活性及其可能的分子机理。方法:水提醇沉、Sevage法除蛋白制备白及多糖;二氧化硅气管滴注法建立大鼠矽肺模型;通过检测大鼠肺指数及组织病理学变化,结合血清SOD、MDA、NF-κB、IL-1β、PDGF、TGF-β1、TNF-α、HYP含量变化,流式细胞术检测CD3~+、CD4~+、CD8~+T细胞百分含量及CD4~+/CD8~+比值,分析白及多糖药效及作用机理。结果:与模型组比较,白及多糖低(100mg/kg)、高(400 mg/kg)剂量组血清SOD活性显著升高,MDA、NO含量显著降低,CD4~+/CD8~+比值逆转(P<0.01)。除白及多糖高剂量能显著降低血清TNF-α含量外,白及多糖对矽肺大鼠血清炎症细胞因子及HYP水平均无明显影响。组织病理学检查显示,白及多糖未能有效改善肺组织纤维化程度。结论:白及多糖对矽肺大鼠机体抗氧化系统和免疫系统具有良好的调节作用,但不能有效抑制肺纤维化,白及中有效抑制肺纤维化活性组分有待进一步研究确证。
OBJECTIVE: To investigate the white fibroin and polysaccharide against silica-induced pulmonary fibrosis in experimental silicosis rats and its possible molecular mechanism. Methods: The polysaccharide and polysaccharide were prepared by water-alcohol precipitation and Sevage method. Silicosis model was established by tracheal instillation. The lung index and histopathological changes of rats were detected. Serum SOD, MDA, NF-κB The percentage of CD3 ~ +, CD4 ~ +, CD8 ~ + T cells and the ratio of CD4 ~ + / CD8 ~ + were detected by flow cytometry. Analysis of white and polysaccharide efficacy and mechanism of action. Results: Compared with the model group, the serum SOD activity was significantly increased and the contents of MDA and NO were significantly decreased and the ratio of CD4 ~ + / CD8 ~ + reversed (P <0.05) in the groups of 100 mg / kg and 400 mg / P <0.01). In addition to high doses of white and polysaccharide can significantly reduce serum TNF-α content, white and polysaccharide on serum inflammatory cytokines and HYP levels in silicosis rats had no significant effect. Histopathological examination showed that white and polysaccharides failed to effectively improve the degree of lung fibrosis. CONCLUSION: WHITE and polysaccharides have a good regulatory effect on the antioxidant and immune systems of silicotic rats, but they can not effectively inhibit pulmonary fibrosis and inhibit the active components of pulmonary fibrosis effectively.