机构地区:[1]上海交通大学附属第一人民医院呼吸科,200080 [2]上海国宝企业发展中心,200001
出 处:《国际呼吸杂志》2011年第9期651-655,共5页International Journal of Respiration
基 金:基金项目:国家“十一五”863计划课题资助项目
摘 要:目的对虫草活力素(简称虫草)在大鼠支气管哮喘(简称哮喘)模型气道重塑中的作用及相关机制进行初步探讨。方法50只Wister大鼠[6~8周龄,(200±20)g],随机数字表法分为阴性对照组(A)、慢性哮喘单纯模型组(B)(卯清白蛋白系统致敏和反复激发)、慢性哮喘+虫草50mg/kg治疗8周组(c)、慢性哮喘+布地奈德(BUD)8周治疗组(D)及慢性哮喘+BUD联合虫草8周治疗组(E)。肺组织切片HE染色观察病理变化并检测气道管壁厚度,采用免疫组织化学法检测气道转化生长因子β1(TGF-β1)表达水平,应用逆转录PCR法检测肺组织A2a腺苷受体(A2aAR)mRNA表达。数据统计采用ANOVA检验进行组间分析,Mann—Whitney检验进行组内两两比较,Spearman等级相关分析。结果①HE染色显示所有药物干预组较单纯模型组炎症细胞浸润、平滑肌肥厚及黏膜肺组织水肿等炎症表现明显减轻,以D和E组最为明显;②5组气道管壁厚度依次分别为(9.89±2.09)、(21.72±3.16)、(14.94±1.96)、(12.29±2.75)和(12.25±2.32)um2/um,F=31.37,P〈0.0001,所有药物干预组气道壁厚度均高于对照组(C组、D组和E组与A组比较后的P值分别为0.0001、0.0524、0.0524),且低于单纯模型组(C组、D组和E组与B组比较后的P值均〈0.0001),差异有统计学意义,C组气道壁较D组和E组增厚,差异有统计学意义(P值分别为0.0232和0.0147);③5组TGF-β1表达强阳性率分别为(2.08±1.63)%、(29.37±5.08)%、(12.30±3.26)%、(10.78±3.35)%及(7.43±2.84)%,F=86.45,P〈0.0001,所有药物干预组TGF-β1蛋白表达均高于对照组(C组、D组和E组与A组比较后的P值均〈0.0001),且低于单纯模型组(C组、D组和E组与B组比较后的P值均〈0.0001),差异有统计学意义;E组较c组的�Objective To investigate the potential suppression role of cordycepin in airway remodeling by observing the expression of transforming growth factor-β1 (TGF-β 1 ) and A2a adenosine receptor (A2aAR) on a rat model of chronic bronchial asthma (asthma). Methods 50 rats were randomized into control group (A), asthma group (B), 50 mg/kg cordycepin treatment group (C), budesonide (BUD) treatment group (D) and combination treatment group (BUD -- cordycepin 50 mg/ kg) (E). After 8 weeks therapy on ovalbumin challenged asthma model, histologic examination were performed to observe the general pathologic alteration and analyze the thickness of airway wall. The protein expressions of TGF-β1 were calculated by immunohistochemistry, and the transcriptions of A2aAR mRNA in the lung tissues were measured by reverse transcriptase polymerase chain reaction (RT-PCR). Data were evaluated using One way ANOVA followed by Turke/s test and Mann-Whitney test. Results (1) HE staining showed that compared with the treatment groups, there were a large number of inflammatory ceils infiltration, heavier smooth muscle hypertrophy and mucous membrane hyperemia in the asthma group. (2) The thickness of airway in each group was (9.89±2.09), (21.72± 3.16), (14.94±1.96),(12.29±2.75) and (12.25±2.32) um2/um respectively, F =31.37, P 〈0.000 1, airway thickness in group C, D and E were all significantly higher than group A ( P =0. 000 1,0. 052 4 and 0. 052 4 respectively), and lower than group B ( P 〈 0. 000 1). Airway in group C also showed remarkably thicker than group D and E ( P = 0. 023 and 0. 015 respectively). (2) The expressions of TGF-β1 in each group was (2.08±1.63) %,(29.37±5.08) %, (12.30±3.26) %,(10.78±3.35) and (7.43±2.84) % respectively, F =86.45, P 〈0.000 1,protein expressions in group C, D and E were all higher than group A ( P 〈0. 000 1, d0. 000 1 and =0. 000 1 respectively), and lower than group B s
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