高迁移率族蛋白1在内毒素性急性肺损伤大鼠肺血管重构中的作用  

Role of high mobility group protein box 1 in pulmonary vascular remodeling in a rat model of acute lung injury

作　　者：王焕亮[1] 彭丽萍[1] 孙满意[1] 陈文娟[1] 类维富[1] 孙宝拄[1] 吴剑波[1] 张文华[2] 

机构地区：[1]山东大学齐鲁医院麻醉科,济南市250012 [2]山东大学齐鲁医院神经外科,济南市250012

出　　处：《中华麻醉学杂志》2012年第10期1278-1280,共3页Chinese Journal of Anesthesiology

基　　金：山东省自然科学基金（Y2007C115,2009ZRB14031,2011ZRE27223,JQ200808）

摘　　要：目的评价高迁移率族蛋白1（HMGBl）在内毒素性急性肺损伤大鼠肺血管重构中的作用。方法健康清洁级雄性Wistar大鼠30只，体重220～250g，采用随机数字表法，将大鼠随机分为3组（n=10）：对照组（C组）、内毒素性急性肺损伤模型组（M组）和HMGBl抗体组（H组）。C组尾静脉输注生理盐水5ml／1．5h；M组输注生理盐水3ml／1．0h，再输注LPS2ml（1mg／kg）／0．5h；H组于注射LPS后12、24和36h时尾静脉注射HMGBl抗体2mg／kg。于注射LPS后72h时处死取肺，光镜下观察肺组织病理学结果，采用图像分析软件测量并计算肺小动脉中膜，血管面积百分比，免疫组化法检测肺血管增殖细胞核抗原（PCNA）表达，Westernbolt法检测HMGBl表达。结果与c组比较，M组和H组肺小动脉中膜／血管面积百分比、PCNA和HMGBl表达水平升高（P〈0．05），肺组织急性炎症细胞增多，血管壁明显增厚；与M组比较，H组肺小动脉中膜，血管面积百分比、PCNA和HMGBl表达水平降低（P〈0．05），肺组织急性炎症和血管壁增厚明显减轻。结论HMGBl可能是诱发内毒素性急性肺损伤大鼠肺血管重构的重要因素。Objective To investigate the role of high mobility group protein box 1 （HMGB1） in pulmonary vascular remodeling in a rat model of acute lung injury （ALl）. Methods Thirty healthy pathogen free male Wistar rats weighing 220-250 g were randomly divided into 3 groups （ n = 10 each） ： group control （group C） ; group LPS （group M） and group LPS ＋ HMGB1 antibody （group H）. The animals were anesthetized with intraperitoneal 10% chloral hydrate 7 ml/kg. ALl was induced with LPS 1 mg/kg infused iv over 30 min in groups M and H. In group H HMGB1 antibody 2 mg/kg was injected iv at 12, 24 and 36 h after LPS administration respectively. The animals were sacrificed at 72 h after LPS administration. The left lung was removed for microscopic examination, measurement of the thickness of the medial layer （tunica media） of pulmonary arterioles and determination of the expression of PCNA （by immune-histochemistry） and HMGB1 protein （by Western blotting）. Results The medial layer of pulmonary arterioles was significantly thicker and the expression of PCNA and HMGB1 higher in group M than in group C. LPS also induced significant inflammatory cell infiltration within the alveoli and damage to the septa. In group H HMGB1 antibody significantly attenuated the above-mentioned LPS-induced changes. Conclusion HMGB1 may play an important role in the LPS-induced pulmonary vascular remodeling.

关 键 词：高迁移率族蛋白质类 呼吸窘迫综合征 成人 内毒素血症 肺血管重构 

分 类 号：R285.5[医药卫生—中药学]