半乳凝素-3对哮喘豚鼠肺组织嗜酸性粒细胞凋亡及Bcl-2蛋白表达的影响

Influence of galectin-3 on apoptosis of eosinophils and expression of Bcl-2 protein in lung tissue of asthmatic guinea pigs

目的:探讨半乳凝素-3对哮喘豚鼠肺组织嗜酸性粒细胞凋亡及Bcl-2蛋白表达的影响。方法:36只豚鼠随机分为哮喘组、治疗组及对照组,每组12只。哮喘组及治疗组用卵白蛋白致敏和激发制作哮喘模型,对照组同期予生理盐水。于致敏第15～21日激发前1h治疗组豚鼠予半乳凝素-3腹腔注射,剂量0.5mg/kg,每日1次,连续7d。测定3组豚鼠支气管肺泡灌洗液(BALF)中IL-5含量、嗜酸性粒细胞计数,苏木素-伊红染色观察肺组织病理变化,TUNEL法检测肺组织嗜酸性粒细胞的凋亡,免疫组织化学检测肺组织Bcl-2蛋白的表达。结果:治疗组豚鼠BALF中IL-5含量和嗜酸性粒细胞计数均低于哮喘组(P<0.05);其肺组织炎症反应明显轻于哮喘组,肺组织嗜酸性粒细胞计数低于哮喘组,嗜酸性粒细胞凋亡指数高于哮喘组;肺组织Bcl-2蛋白表达低于哮喘组(P<0.05)。与对照组比较,治疗组BALF中白细胞计数、嗜酸性粒细胞计数、嗜酸性粒细胞占白细胞的比例、IL-5水平均升高(P<0.05或0.01);肺组织嗜酸性粒细胞计数、嗜酸性粒细胞凋亡指数均显著升高(P均<0.01);肺组织Bcl-2蛋白表达比较差异无统计学意义(P>0.05)。结论:半乳凝素-3可促进哮喘豚鼠BALF中嗜酸性粒细胞凋亡,减轻肺组织炎症反应,这可能与其降低哮喘豚鼠BALF中IL-5含量、下调肺组织Bcl-2蛋白表达有关。

Objective：To study the influence of galectin-3 on apoptosis of eosinophils and Bcl-2 protein expression in lung tissue of asthmatic guinea pigs. Methods： Thirty-six guinea pigs were randomly divided into saline group, asthma group and galectin-3 group （n=12）. Asthma model was created with ovalbumin （OVA）. Galectin-3 （0.5 mg/kg） was injected intraperitoneally daily 1 hour before stimulation during the 15th to 21st day of sensitization in galectin-3 group. Interleukin 5 （IL-5） level and eosinophil counts in bronchoalveolar lavage fluid （BALF） were determined. Pulmonary pathological change was observed. Apoptosis of eosinophils and expression of Bcl-2 protein in lung tissue were detected by TUNEL method and immunohistochemistry, respectively. Results：Compared with asthma group, IL-5 level and eosinophil counts in BALF were significantly lower in galectin-3 group （P0.05）. Furthermore, significantly milder inflammatory reaction was observed in lung tissue in galectin-3 group than that in asthma group, with higher eosinophilic apoptosis index and lower expression level of Bcl-2 protein （P0.05）. Conclusion：Galectin-3 can reduce the eosinophil counts in BALF and inflammation in lung tissue of asthmatic guinea pigs via reducing IL-5 level in BALF, inhibiting Bcl-2 protein expression and promoting eosinophilic apoptosis.