摘要
目的 研究雷公藤甲素对支气管哮喘（简称哮喘）小鼠肺组织中信号转导和转录激活因子-1（STAT-1）与细胞间黏附分子-1（ICAM-1）表达的影响,探讨其治疗哮喘的机制.方法 40只雄性昆明小鼠随机分成4组：正常对照组、哮喘组、地塞米松治疗组及雷公藤甲素治疗组,以卵清蛋白致敏和激发方法建立哮喘小鼠动物模型并给予相应治疗.24 d后处死小鼠,检测BALF中白细胞总数及嗜酸粒细胞（EOS）计数;采用逆转录-聚合酶链反应（RT-PCR）方法检测肺组织中STAT-1、ICAM-1 mRNA表达水平;采用免疫组织化学法检测肺组织中STAT-1、ICAM-1蛋白表达水平.结果 哮喘组STAT-1、ICAM-1 mRNA及蛋白表达明显高于正常对照组（P＜0.01）,雷公藤甲素治疗组及地塞米松组明显低于哮喘组（P＜0.01）.肺组织STAT-1蛋白的表达与BALF中白细胞数、EOS计数及肺组织ICAM-1蛋白表达呈正相关（r分别为0.665,0.735,0.677,P＜0.01）.肺组织ICAM-1蛋白表达与白细胞总数、EOS计数呈正相关（r分别为0.792,0.776,P＜0.01）.结论 雷公藤甲素抑制哮喘气道炎症的机制可能与其抑制STAT-1与ICAM-1的表达活性有关.
Objective To study the effects of triptolide on the expression of STAT-1 and ICAM-1 in asthmatic mice,and to explore the possible therapeutic mechanism of triptolide in asthma.Methods Forty Kunming male mice were randomly divided into 4 groups：control group,asthmatic group,dexamethasone group and triptolide group.The asthmatic model was established by ovalbumin injection and ihalation.And the 4 groups were treated respectively with normal saline （as control）,dexamethasone or triptolide.Twenty-four days later,the mice were executed.The numbers of total leukocytes and eosinophils in bronchoalveolar lavage fluid （BALF） were counted by optical microscope.RT-PCR was employed to detect the mRNA of STAT-1 and ICAM-1 in the lung tissue.The protein of STAT-1 and ICAM-1 expression were measured by immunohistochemistry.Results STAT-1 and ICAM-1 mRNA and the protein expression in lung tissue of asthmatic group significantly increased compared with those of control group （P 〈0.01）.The mRNA and protein expression of STAT-1 and ICAM-1 in mice treated with triptolide and dexamethasone were significantly lower than those in asthmatic group （P 〈0.01）.STAT-1 protein expression in lung tissue was correlated with the number of total leukocytes and eosinophils in BALF and protein expression of ICAM-1 （r =0.665,0.735 and 0.677,P 〈0.01,respectively）.ICAM-1 protein expression in lung tissue was correlated with the number of total leukocytes and eosinophils in BALF （r =0.792 and 0.776,P 〈0.01,respectively）.Conclusions The mechanism of triptolide inhibiting asthmatic airway inflammation may be related to its inhibiting activities of STAT-1 and ICAM-1.
出处
《国际呼吸杂志》
2014年第13期961-966,共6页
International Journal of Respiration
