黎氏哮喘Ⅰ号方对哮喘小鼠嗜酸性粒细胞凋亡及bcl-2基因表达的影响

Influence of Li's Prescription Ⅰ for Asthma on Apoptosis of Eosinophils and Expression of Bcl-2 Gene in Asthmatic Mice

【目的】通过观察黎氏哮喘Ⅰ号方对哮喘小鼠肺组织嗜酸性粒细胞(EOS)凋亡及bcl-2基因表达的影响,进一步探讨哮喘Ⅰ号方治疗哮喘的作用机制。【方法】采用卵白蛋白(OVA)腹腔注射致敏与雾化吸入激发的方法复制小鼠支气管哮喘模型。将60只符合实验标准的SPF级雄性昆明小鼠随机分为6组:正常组,哮喘模型组,地塞米松组(剂量为2 mg/kg),哮喘Ⅰ号方低、中、高剂量组(剂量分别为6.4、12.8、19.2 g.kg-1.d-1),每组10只。正常组采用生理盐水代替OVA,处理程序同哮喘模型组。采用DNA末端原位标记法和免疫组化法观察各组小鼠肺组织EOS凋亡基因及凋亡抑制基因bcl-2的表达情况。【结果】哮喘Ⅰ号方各剂量组肺组织中EOS凋亡指数显著高于哮喘模型组(P<0.01),并可显著抑制肺组织EOS凋亡抑制基因bcl-2的表达(P<0.05或P<0.01)。【结论】哮喘Ⅰ号方治疗哮喘的机理与抑制凋亡抑制基因bcl-2的表达,促进EOS凋亡,从而减轻炎症的高反应状态有关。

Objective To study the influence of Li’s Prescription Ⅰfor Asthma（LPAⅠ）on apoptosis of eosnophils（EOS）in lung tissue of asthmatic mice,and to explore its possible therapeutic mechanism for asthma.Methods Sixty Kunming male mice with specific pathogen free were equally randomized into 6 groups：normal group,model group,dexamethasone group（2mg/kg）,and low-,middle-and high-dosage LPAⅠ groups（in the dose of 6.4,12.8 and 19.2 g·kg-1·d-1,respectively）.Mice models of bronchial asthma were induced by sensitization with intraperitoneal injection of ovalbumin（OVA）and challenge with nasal inhalation of OVA.The expression of apoptosis gene and anti-apoptosis gene bcl-2 in EOS of mice lung tissue was detected with in situ DNA end-labeling technique and immunohistochemical assay.Results EOS apoptotic index was higher（P〈0.01）,and bcl-2 expression level in EOS was lower（P〈0.05 or P〈0.01）in LPAⅠ groups than those in the model group.Conclusion The therapeutic mechanism of LPAⅠ for bronchial asthma is possibly related with inhibiting bcl-2 expression,promoting apoptosis of EOS and reducing hyperreactive inflammation in lung tissue of asthmatic mice.