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作 者:徐笑益[1] 石卓[2] 鲍军明[1] 顾伟忠[2] 姚航平[3] 陈智[3] 高敏[4] 方向明[5]
机构地区:[1]浙江大学医学院附属邵逸夫医院麻醉科,浙江杭州310016 [2]浙江大学医学院附属儿童医院儿科研究所,浙江杭州310003 [3]浙江大学医学院附属第一医院传染病研究所,浙江杭州310003 [4]浙江大学医学院附属邵逸夫医院临床实验室,浙江杭州310016 [5]浙江大学医学院附属第一医院麻醉科,浙江杭州310003
出 处:《浙江大学学报(医学版)》2006年第6期600-604,共5页Journal of Zhejiang University(Medical Sciences)
基 金:国家自然科学基金资助项目(30070854)
摘 要:目的:观察重组β-防御素2多肽预处理对脓毒症大鼠肺组织细胞凋亡的影响。方法:SPF级SD大鼠48只随机分成对照组和防御素组,采用盲肠结扎穿孔术(CLP)复制脓毒症模型,防御素组在CLP前48h经气管插管气道滴注107PFU重组腺病毒(含有β-防御素2编码基因),而对照组则同法给予对照腺病毒(不含β-防御素2编码基因)。分别于CLP后0、12、36和72 h处死大鼠,取肺组织,采用透射电镜,末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测细胞凋亡,采用电镜、苏木精-伊红(HE)染色观察肺组织病理变化。结果:TUNEL检测显示,对照组大鼠CLP后12、36和72 h肺组织细胞凋亡指数显著增加(P<0.01);与对照组相比,防御素组CLP后相应时间点肺组织细胞凋亡指数显著降低(P<0.05)。HE染色可见,两组大鼠CLP后12、36和72 h肺泡及肺泡间质充血、水肿,炎症细胞渗出,肺泡腔不同程度狭窄。与对照组相比较,防御素组相应时间点肺组织内炎症细胞渗出减少,间质水肿减轻。结论:重组β-防御素2多肽预处理能抑制脓毒症肺组织的细胞凋亡,对急性肺损伤(AL I)具有保护作用。Objective. To investigate the effect of recombinant β-defensin 2 (BD-2) on the apoptosis of pulmonary tissue in rats with sepsis. Methods: Forty-eight SD rats were randomly divided into defensin group and controls. In control group 24 rats received 10^7PFU adenovirus via trachea intubation. In defensin group 24 rats received 10^7PFU recombinant adenovirus carrying all expression cassette of rat BD-2 (Ad-rBD2). All rats received cecal ligation and puncture (CLP) to induce sepsis 48 h following the administration of adenovirus. Rats of both groups were sacrificed at 0, 12, 36 and 72 h after CLP; lungs were removed and fixed for Haematoxylin and Eosin (HE) stain. Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) technique. Results: The apoptosis index (AI) of lung cells increased significantly following CLP in control group, while it was significantly lower in defensin group than that of control group (P〈0.05). In addition, a significant alveolar damage, interstitial edema, and infiltration of inflammatory cells were observed in control lungs, while it was less severe in defensin group. Conclusion: Recombinant β-defensin 2 may reduce the apoptosis of lung cells and attenuate lung injury.
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