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作 者:李金田[1] 李娟[1] 刘永琦[1] 陈珺明[2] 程小丽[1] 楚惠媛[1] 颜春鲁[1]
机构地区:[1]甘肃中医学院,甘肃兰州730000 [2]石河子大学第一附属医院,新疆石河子832006
出 处:《中成药》2007年第1期33-36,共4页Chinese Traditional Patent Medicine
基 金:国家教育部科学技术研究重点项目(02146);甘肃省中医药管理局科学研究项目基金资助项目(2002-GZK-37)
摘 要:目的:探讨平喘灵冲剂对哮喘的治疗作用及其机制。方法:用卵蛋白雾化吸入致敏法,复制大鼠哮喘模型;将SD大鼠分为空白对照组、哮喘模型组、地塞米松组、平喘灵大、小剂量组,共5组;取血清及肺泡灌洗液进行嗜酸性粒细胞(Eos)计数,肺组织制作切片HE染色形态学观察,并采用免疫组织化学法技术检测肺组织Fas、Bcl-2的表达。结果:模型组较空白组血液中和肺泡灌洗液(BALF)中Eos的数量均明显升高,引喘潜伏期明显缩短(P<0.05),组织形态学病变明显,气道Eos等炎症细胞Fas、Bcl-2表达异常;激素组及平喘灵大剂量治疗组较模型组血液中和BALF中Eos的数量明显降低,引喘潜伏期明显延长(P<0.05),组织形态学改善明显,并可纠正气道Eos等炎症细胞Fas、Bcl-2的异常表达(P<0.05)。结论:平喘灵可通过调节气道Eos炎症细胞Fas、Bcl-2的异常表达从而达到治疗哮喘的目的。AIM: To study the therapeutic effects and the related mechanism of Pingchuanling(PCL) on bronchial asthma in rats. METHODS : The rats asthma model was established by ovalbumin (OVA) sensitization. The SD rats were divided into the normal control group, asthma model group, dexamethasone group, low and higher dose of PCL group. Eos in serum and BALF were taken count of and tissue slice dyed with HE were observed. In addition Fas, Bcl-2 expression in lung tissue were examined by immunotisssuchemical technology. RESULTS: Eos count in serum and BALF of asthma model group were increased significantly as compared with that in normal animals. Asthma induced delitescence also were shorten obviously, the differences between the groups were all significant ( P 〈 0.05 ). Morphologic pathological change was also distinct and Fas, Bcl-2 expression of Eos of trachea was abnormal. After being treated amount of Eos in serum and BALF were decreased significantly in dexamethasone group and high dose of PCL group and asthma induced delitescence were prolonged obviously as compared with that in model animals ( P 〈 0.05 ). At the same time morphologic pathological improvment was also distinct and abnormal expression of Fas, Bcl-2 in Eos of trachea were corrected, the differences between the groups were all significant (P 〈 0.05 ). CONCLUSION: PCL has therapeutic effects on bronchial asthma by regulating the expression of Fas, Bcl-2 in Eos inflammatory cells of trachea.
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