黄芪多糖对慢性阻塞性肺疾病大鼠肺组织内基质金属蛋白酶-9、金属基质蛋白酶抑制剂-1表达的影响(1)
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[摘要] 目的 观察黄芪多糖(ASP)对慢性阻塞性肺疾病(COPD)大鼠肺组织内基质金属蛋白酶-9(MMP-9)和金属基质蛋白酶抑制剂-1(TIMP-1)表达的影响。 方法 Wistar雄性大鼠40只，随机分为4组：正常对照组，COPD组，黄芪多糖组，强的松组；采用改良烟熏加气管内滴加脂多糖(LPS)方法复制COPD模型，黄芪多糖组采用黄芪多糖灌胃干预30 d，强的松组采用强的松灌胃干预30 d，其他组用等剂量生理盐水灌胃。此后检测各组动物肺功能，取肺组织观察其病理学变化，分别检测各组肺组织中羟脯氨酸(MPO)含量，MMP-9、TIMP-1蛋白的水平，计算MMP-9/TIMP-1比值。 结果 COPD组呈现慢性阻塞性肺组织病理变化，肺功能减低，MPO、MMP-9、TIMP-1表达增加，MMP-9/TIMP-1比值增高；黄芪多糖和强的松干预后，肺组织病理改变好转，肺功能改善，MPO、MMP-9、TIMP-1表达减低，MMP-9/TIMP-1比值降低，0.2 s用力呼吸量/用力肺活量(FEV0.2/FVC)与MMP-9/TIMP-1比值呈负相关。 结论 黄芪多糖可通过抑制COPD大鼠肺组织MMP-9、TIMP-1的表达，改善肺组织损伤及肺功能。
[关键词] 慢性阻塞性肺病；黄芪多糖；基质金属蛋白酶-9；金属基质蛋白酶抑制剂-1
[中图分类号] R56 [文献标识码] A [文章编号] 1673-7210(2012)01(b)-025-03
Effect of astragalus polysaccharide on the expression of MMP-9 and TIMP-1 in lung tissue of COPD rats
YU Weiwei HUANG Xiaoyan ZHANG Yan XIA Qin▲
Department of General, Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Hubei Province, Wuhan 430030, China
[Abstract] Objective To observe the influence of astragalus polysaccharide (ASP) on the expression level of MMP-9 and TIMP-1 in lung tissue of chronic obstructive pulmonary disease (COPD) rats. Methods 40 male Wistar rats were randomly divided into four groups, Normal group, COPD group, ASP group and prednisone group. The model of COPD was established by smoking method combined with endotracheal injection of lipopolysaccharide. After the drugs were administrated for 30 days，the lung function of rats were determined. The lung content of hydroxyproline was detected by biochemicaly method. The protein content of MMP-9 and TIMP-1 was determined semi-quantitatively by immunohistochemical methods. Results The COPD group showed chronic obstructive pulmonary histopathologic change, the lung function decreased, the expression MPO, MMP-9 and TIMP-1 increased, MMP-9/TIMP-1 decreased; after intervention of ASP and prednisone, the pulmonary histopathologic change and the lung function improved, the expression MPO, MMP-9, TIMP-1 and MMP-9/TIMP-1 decreased, there was a negative correlation between FEV0.2/FVC and MMP-9/TIMP-1. Conclusion ASP can effectively inhibit the expression of MMP-9 and TIMP-1, improve the lung function and ECM imbalance of degradation and sedimentary, and delay airway remodeling ......
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