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P27通过调控Bcl―2对哮喘大鼠气道平滑肌重塑影响
P27通过调控Bcl―2对哮喘大鼠气道平滑肌重塑影响
[摘要] 目的 观察P27kip-1(以下简称P27)是否通过调控Bcl-2影响哮喘大鼠气道重塑的发生发展。 方法 SPF级雄性大鼠30只随机分成正常对照组和哮喘组,各15只。用卵白蛋白(OVA)致敏和激发的方法制备哮喘模型。观察各组大鼠肺组织病理超微结构变化,分析支气管肺泡灌洗液(BALF)中的细胞分类计数,并采用免疫组化法测定各组大鼠肺组织中P27、Bcl-2表达情况。 结果 哮喘组嗜酸粒细胞计数比例均显著高于对照组(P0.01),哮喘组肺组织P27表达低于对照组(P0.01),哮喘组肺组织Bcl-2表达高于对照组(P0.01)。 结论 P27通过调控Bcl-2抑制气道平滑肌细胞增生进而影响气道重塑。
[关键词] 哮喘;P27;Bcl-2;气道重塑
[中图分类号] R562.25 [文献标识码] A [文章编号] 1673-9701(2017)34-0028-04
Effect of P27 on airway smooth muscle remodeling in asthmatic rats by regulating Bcl-2
XU Hui LEI Dan PENG Yanping DAI Yuanrong
Department of Respiratory Diseases, Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China
[Abstract] Objective To investigate whether P27kip-1(hereinafter referred to as P27) regulates the development of airway remodeling in asthmatic rats via Bcl-2. Methods 30 SPF male rats were randomly divided into normal control group(n=15) and asthma group(n=15). Asthma models were prepared by sensitization and challenge with ovalbumin (OVA). The pathological and ultrastructural changes of lung tissue in each group were observed. The cell differential count in bronchoalveolar lavage fluid(BALF) was analyzed. The expressions of P27 and Bcl-2 in lung tissue of each group were detected by immunohistochemistry. Results The percentage of eosinophil count in asthma group was significantly higher than that in control group(P0.01). The expression of P27 in lung tissue of asthma group was lower than that in control group(P0.01). The expression of Bcl-2 in lung tissue of asthma group was higher than that in control group(P0.01). Conclusion P27 inhibits airway smooth muscle cell proliferation and thus affects airway remodeling through the regulation of Bcl-2.
[Key words] Asthma; P27; Bcl-2; Airway remodeling
支气管哮喘(哮喘)发病的病理基础为气道重塑,目前对于改善或延缓气道重塑缺乏有效对策。近年来,研究发现气道平滑肌细胞(ASMC)重塑和凋亡失衡导致了支气管哮喘的发生发展[1,2]。凋亡是在基因控制下,细胞自主、有序的死亡过程[3]。P27kip-1(以下简称P27)为细胞周期负性调节因子,分子量约27 kD,主要定位于细胞核,通过抑制周期蛋白E-周期蛋白依赖激酶2(cyclinE-CDK2)
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