摘要
目的:观察失血性休克复合内毒素(LPS)二次打击大鼠肺泡毛细血管内皮细胞膜水通道蛋白1(AQP1)的表达变化及人参二醇皂苷(PDS)和糖皮质激素(Dex)对其影响。方法:通过失血性休克复合LPS二次打击建立稳定的急性肺损伤模型,分为假手术对照组(S)、二次打击模型组(HL)、Dex预治疗组(HLD)及PDS预治疗组(HLP);应用HE染色观察肺组织病理学变化,采用RT-PCR、Western blotting及免疫组织化学检测AQP1的表达。结果:①病理组织学结果显示,HL组肺组织可见较弥漫的间质炎性改变,肺泡间隔明显增宽,肺间质内有大量的炎性细胞浸润,可见灶性出血,肺泡腔变小,部分腔内含有水肿液;而HLD组及HLP组大鼠肺脏改变明显减轻。②HL组肺组织AQP1 mRNA及蛋白表达水平均低于其他各组(P<0.05);免疫组织化学检测,肺泡周围毛细血管内皮细胞AQP1呈弱阳性,而HLD组及HLP组AQP1 mRNA及蛋白表达量明显高于HL组(P<0.05)。结论:失血-LPS二次打击可使大鼠肺组织中AQP1的表达减少,加重肺损伤,是肺水肿形成的原因之一;Dex与PDS能使其表达提高,从而起到减轻肺水肿的作用;PDS与Dex有减轻失血性休克复合内毒素二次打击诱导的肺损伤作用。
Objective To investigate the alteration of aquaporin 1 （AQP1） expression in lung tissues in hemorrhage-lipopolysaccharide （LPS） two-hits rats and the effects of panaxadiols （PDS） and dexamthasone （Dex） on it. Methods The rat model of acute lung injury was built with hemorrhage-LPS two hits. The experiment was divided into control group （S）, two-hits model group （HL）, DEX group （HLD）, and PDS group （HLP）. The pathological changes of lung tissue were examined by HE staining. The expression of AQP1 was analyzed by RT-PCR, Western blotting and immunohistochemical staining. Results ① Significant inflammatory changes in pulmonary interstitial of rats in HL group were observed. However, in HLD group and HLP group, the pulmonary pathologic changes were much slighter. ② AQP1 mRNA and protein expressions in lung tissues in HL group were significantly decreased compared with others groups （P〈0.05）, immunohistochemistry analysis got the similar result. Positive AQP1 expression in the endothelium of capillary vessels on the wall of alveolus was merelv very weak exDression in HL group. AQP1 mRNA and protein expression levels in lung tissues in HLD group and HLP group were significantly higher than those in HL group （P〈0.05） . Conclusion The hemorrhage-LPS two hits can inhibit the expression of AQP1, while PDS could increase AQP1 expression in lung tissue, lighten the edema, and maintain the intact structure of lung tissue.
出处
《吉林大学学报（医学版）》
CAS
CSCD
北大核心
2008年第3期449-452,F0003,共5页
Journal of Jilin University：Medicine Edition
基金
吉林省科技厅自然科学基金资助课题(20030551-3)
