活化过氧化物酶体增殖激活物受体γ对烟熏肺气肿大鼠肺血管炎症的影响

发布时间：2018-04-24 15:24

本文选题：肺气肿 + 血管炎　；参考：《中国现代医学杂志》2014年05期

【摘要】：目的观察过氧化物酶体增殖激活物受体γ(PPARγ)活化后对烟熏肺气肿大鼠肺血管炎症的影响。方法将40只SPF级雄性大鼠按照随机数字表法分为空白组、模型组、罗格列酮组(R组)、罗格列酮+BADGE组(RB组),每组10只。采用烟熏12周的方法复制肺气肿大鼠模型。观察4组大鼠肺血管的变化,免疫组织化学检测PPARγ和金属基质蛋白酶9(MMP-9)在肺血管上的表达。多组间比较采用单因素方差分析,组间两两比较采用SNK-q检验,采用直线相关分析进行相关性检验。结果模型组和RB组大鼠肺血管中大量炎症细胞浸润,血管重塑明显,肺血管炎症细胞浸润程度模型组(212.35±21.24)/0.01 mm2和RB组(200.37±32.35)/0.01 mm2明显高于空白组(26.81±4.93)/0.01 mm2和R组(101.23±22.44)/0.01 mm2(均P0.01),肺血管重塑程度模型组(1.65±0.53)和RB组(1.49±0.63)明显高于空白组(0.25±0.04)和R组(0.53±0.05)(均P0.01),肺血管炎症细胞浸润和肺血管重塑呈正相关(r=0.903,P0.01);肺血管上PPARγ蛋白(平均光密度值)表达R组(0.311±0.022)明显高于模型组(0.234±0.013)、RB组(0.237±0.012)和空白组(0.279±0.003)(均P0.01),MMP-9表达模型组(0.418±0.014)和RB组(0.411±0.011)明显高于空白组(0.356±0.021)和R组(0.376±0.004)(均P0.01),PPARγ与MMP-9表达呈负相关(r=-0.643,P0.01)。结论烟熏肺气肿大鼠肺血管炎症和血管重塑明显,活化PPARγ有抑制MMP-9、减轻肺血管炎症和血管重塑作用。
[Abstract]:Objective to observe the effect of peroxisome proliferator receptor 纬 (PPAR 纬) activation on pulmonary vascular inflammation in rats with fumigated emphysema. Methods Forty SPF male rats were randomly divided into control group, model group, rosiglitazone group R group and rosiglitazone BADGE group with 10 rats in each group. Emphysema rat model was established by smoking for 12 weeks. The changes of pulmonary blood vessels and the expression of PPAR 纬 and metalloproteinase 9 (MMP-9) in pulmonary vessels were detected by immunohistochemistry. Single factor analysis of variance (ANOVA) was used for multigroup comparison, SNK-q test was used for intergroup comparison, and linear correlation analysis was used for correlation test. Results in the model group and RB group, a large number of inflammatory cells infiltrated the pulmonary vessels, and the vascular remodeling was obvious. The infiltration degree of pulmonary vascular inflammatory cells in the model group (212.35 卤21.24 mm2) and RB group (200.37 卤32.35% / 0.01 mm2) was significantly higher than that in the blank group (26.81 卤4.93g / 0.01 mm2) and R group (101.23 卤22.44g / 0.01 mm ~ (2)) (all P 0.01g, 1.65 卤0.53) and RB (1.49 卤0.63) were significantly higher than those in the blank group (0.25 卤0.04) and R group (0.53 卤0.05) (P 0.011, P 0.011, respectively). The expression of PPAR 纬 protein (mean optical density) in group R was significantly higher than that in model group (0.234 卤0.013) and blank group (0.279 卤0.003) (all P0.011 卤0.014) and RB (0.411 卤0.011 卤0.011) significantly higher than that in model group (P 0.011 卤0.011). There was a negative correlation between the expression of PPAR- 纬 and MMP-9 in R group and R group (P < 0. 356 卤0. 021) and R group (P = 0. 376 卤0. 004). Conclusion Pulmonary vascular inflammation and vascular remodeling were obvious in fumigated emphysema rats. Activation of PPAR 纬 inhibited MMP-9 and alleviated pulmonary vascular inflammation and vascular remodeling.
【作者单位】：中国医科大学附属第一医院呼吸疾病研究所;
【分类号】：R563.3

【共引文献】