山莨菪碱治疗兔创伤性急性肺损伤分子生物学机制的实验研究  

Molecular biological mechanism of anisodamine in treatment of acute traumatic lung injury in rabbits

作　　者：简文[1] 樊爱琳[2] 尹文[3] 戚好文[1] 柏长青[4] 

机构地区：[1]第四军医大学西京医院呼吸内科,陕西西安710033 [2]第四军医大学西京医院检验科,陕西西安710033 [3]第四军医大学西京医院急诊科,陕西西安710033 [4]解放军第307医院呼吸内科,北京100071

出　　处：《第四军医大学学报》2008年第11期985-987,共3页Journal of the Fourth Military Medical University

摘　　要：目的：探讨山莨菪碱（654-2）对家兔创伤性急性肺损伤（ALI）治疗作用的分子生物学机制.方法：采用创伤性急性肺损伤模型,将家兔随机分为对照组（CG）,肺损伤组（IG）和治疗组（EG）,每组24只.各组动物分别于肺损伤模型建立后1,2,3,4h各放血处死6只,留取支气管肺泡灌洗液（BALF）,分离肺泡巨噬细胞（PAM）,用凝胶电泳迁移率改变分析法（EMSA）和RT-PCR法检测PAM中NF-κB的活性变化及TNF-α mRNA的表达水平,用ELISA法检测BALF上清中TNF-α和IL-8的含量.结果：IGNF-κB活性、TNF-αmRNA表达及TNF-α,IL-8含量于模型建立后1～4h内均明显高于CG（P〈0.01）;EG经山莨菪碱治疗后上述指标与IG相比均有明显下降（P〈0.01,P〈0.05）.结论：山莨菪碱对ALI有治疗作用,此作用与其对NF-κB活性及TNF-αmRNA,TNF-α,IL-8表达抑制有关.AIM： To investigate the molecular biological mechanism of anisodarnine in the treatment of traumatic acute lung injury （ALI） in rabbits. METHODS： Rabbits were randomly divided into 3 groups： control group （CG） , injury group （IG） and experimental group （EG） , with 24 in each group. The rabbits in IG and EG were given LPS after being impacted to make traumatic ALI After the ALI model was made, the rabbits of EG were intravenously injected with anisodamine. Every 6 rabbits in each group were killed at 1, 2, 3 and 4 h after the model was established. Bronchoalveolar lavage fluid （BALF） was collected in order to isolate pulmonary alveolar macrophages （ PAM ）. The NF-κB activity of PAM and the expression of TNF-αmRNA in PAM were measured by electrophoretic mobility shift assay （EMSA） and semi-quantity reverse transcription PCR （RT- PCR）. The levels of TNF-α and IL-8 in BALF were measured by ELISA. RESULTS： Compared with CG, the activity of NF-KB, expression of TNF-α mRNA and levels of TNF-α, IL-8 in BALF were obviously increased in IG during 1 - 4 h （ P 〈 0.01 ）. In EG, the above indexes were significantly lower than those in IG （P〈0.01, P 〈 0.05）. CONCLUSION： Anisodamine has therapeutic roles in traumatic ALI, which is closely related to its inhibitory effects on the NF-KB activation and pro-inflammatory factor secretion.

关 键 词：山莨菪碱 创伤 急性肺损伤 核因子-ΚB 细胞因子 

分 类 号：R655[医药卫生—外科学]