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目的:探讨哮喘时肺组织炎症、中性粒细胞(PMN)、肺泡Ⅱ型(AT-Ⅱ)细胞等的病理改变和转化生长因子-β_1(TGF-β_1)的表达及地塞米松对其的影响。方法:建立哮喘大鼠模型,支气管肺泡灌洗液(BALF)行细胞计数,光镜、电镜观察肺组织病理改变,免疫组化法检测肺组织TGF-β_1的表达。结果:BALF中A组细胞总数、EOS计数显著性高于C组(P<0.01),D组显著性高于C组但低于A组(均P<0.01)。肺组织中A组PMN计数显著性高于C组(P<0.01),D组显著性高于A组(P<0.01)。A组AT-Ⅱ细胞变性、坏死、崩解、板层体空泡化现象。TGF-β_1的表达水平在A组显著性高于C组(P<0.01),D组显著性高于C组但低于A组(分另为P<0.01,0.05)。结论:哮喘大鼠肺组织炎症细胞浸润、气道黏膜损伤、AT-Ⅱ细胞损伤、表达水平增加;地塞米松可减少上述病理改变,但对肺组织中PMN数目有增加作用,可能会加重对肺组织的损伤。
Objective: To investigate the pathological changes of lung tissue inflammation, neutrophil (PMN) and alveolar type Ⅱ (AT-Ⅱ) cells and the expression of transforming growth factor-β 1 (TGF-β 1) in asthmatic rats and the effects of dexamethasone on influences. Methods: The asthmatic rat model was established. The bronchoalveolar lavage fluid (BALF) was taken for cell counting. The pathological changes of lung tissue were observed under light microscope and electron microscope. The expression of TGF-β 1 in lung tissue was detected by immunohistochemistry. Results: The total number of cells in group A and the count of EOS in BALF were significantly higher than those in group C (P <0.01), but significantly higher in group D than those in group C (all P <0.01). The lung tissue PMN count of group A was significantly higher than that of group C (P <0.01), and that of group D was significantly higher than that of group A (P <0.01). A group of AT-Ⅱ cells degeneration, necrosis, disintegration, lamellar body vacuole phenomenon. The expression of TGF-β_1 in group A was significantly higher than that in group C (P <0.01). The level of TGF-β 1 in group A was significantly higher than that in group C but lower than that in group A (P <0.01, 0.05). Conclusion: Inflammatory cell infiltration, airway mucosal injury and AT-Ⅱ cell injury in lung tissue of asthmatic rats are increased. Dexamethasone can reduce the above pathological changes, but may increase the number of PMN in lung tissue, which may aggravate the expression of Lung tissue damage.