甘草酸二铵脂质配体对大鼠急性肺损伤的改善作用及机制  

Ameliorative Effect and Mechanism of Diammonium Glycyrrhizinate Lipid Ligand on Acute Lung Injury in Rats

作　　者：刘梅梅[1] 黄焱平 杨珺[1] LIU Meimei;HUANG Yanping;YANG Jun(Anhui Medical College, Hefei, Anhui 230601,China)

机构地区：[1]安徽医学高等专科学校,安徽合肥230601

出　　处：《九江学院学报（自然科学版）》2021年第4期83-88,105,共7页Journal of Jiujiang University：Natural Science Edition

基　　金：安徽省自然科学研究重点项目(编号KJ2016A374)的成果之一。

摘　　要：目的探讨甘草酸二铵脂质配位体(DGLL)对大鼠急性肺损伤(ALI)的影响及有关机制。方法大鼠灌胃DGLL(30、60、120mg/kg),腹腔内注射内毒素(LPS)建立大鼠ALI模型。模型建立后使用HE染色技术评估各组肺损伤程度。检测肺干湿重比和支气管肺泡灌洗液(BALF)中的蛋白含量;使用肺组织中的Evans蓝(EB)来评估肺水肿。采用ELISA法测定大鼠肺组织中肿瘤坏死因子(TNF-α)和白细胞介素(IL-1β)的表达水平。通过免疫组织化法检测骨髓过氧化物酶(MPO)的表达程度。使用Western blotting法测定血管内皮钙黏蛋白(VE-cadherin)、细胞间粘附分子(ICAM-1)、粘附蛋白ZO-1、JAM-1的表达水平。结果大鼠肺组织中TNF-α、IL-1β和ICAM-1的表达水平以及MPO免疫反应性显著降低。DGLL减轻了EB外渗和BALF的蛋白浓度;血管内皮钙粘蛋白VE-cadherin的表达水平下降;肺组织中的连接蛋白ZO-1、JAM-1的表达水平显著降低。结论DGLL对LPS诱导的大鼠ALI表现出的保护作用与抑制炎细胞的浸润和微血管屏障的破坏有关。Objective To study the effects of diammonium glycyrr-hizinate(DGLL)on acute lung injury(ALI)and pulmonary edema in rats.Method The rat ALI model was established by LPS intraperitoneal injection.Lung injury was evaluated using hematoxylin and eosin staining techniques.Pulmonary edema was evaluated using lung wet-dry weight ratio,protein concentrations in the bronchoalveolar lavage fluid(BALF)and Evans blue(EB)extravasation in lung tissue.The expression levels of tumor necrosis factor(TNF-α)and IL-1βin lung tissues were measured using ELISA.Myeloperoxidase(MPO)expression levels were detected by immunohistochemicalstaining.Western blotting was used to measure the expression level changes of intercellular adhesion molecule(ICAM-1),as well as adherent and tight junction proteins,including vascular endothelial VE-cadherin,zonula occludens ZO-1,occludin and junctional adhesion molecule JAM-1 that were associated with pulmonary inflammation and microvascular permeability.Result DGLL treatment significantly alleviated ALI induced by LPS,which was demonstrated by reduction of MPO-positive cells and expression levels of TNF-α,IL-1βand ICAM-1 in rat lung tissues.DGLL abrogated LPS-induced pulmonary edema,decreased the protein concentration in BALF and reduced EB extravasation.DGLL also reversed the reduced expression of VE-cadherin and tight junction proteins,including ZO-1,occludin and JAM-1 in the lung tissues caused by LPS.Conclusion DGLL exhibited aprotective effect on LPS-induced rat ALI,which was associated with the inhibition of inflammatory cell infiltration and microvascular barrier disruption.

关 键 词：肺损伤 粘附分子 血管内皮钙粘蛋白 紧密连接蛋白 

分 类 号：R91[医药卫生—药学]