芪冬活血饮对急性肺损伤大鼠TLR4/NF-κB炎症信号通路的影响  

The effect of Qidong Huoxue Decoction on TLR4/NF-κB inflammatory signaling pathway in acute lung injury rats

作　　者：洪辉华[1] 杨珺超[1] 高润娣[1] 赵玮[1] 朱渊红[1] 蔡宛如[2] 

机构地区：[1]浙江中医药大学附属第一医院呼吸科,浙江杭州310006 [2]浙江中医药大学附属第二医院呼吸科,浙江杭州310005

出　　处：《温州医学院学报》2015年第5期332-337,共6页Journal of Wenzhou Medical College

基　　金：国家自然科学基金资助项目(81273678);浙江省自然科学基金资助项目(LQ12H29003)

摘　　要：目的:通过观察芪冬活血饮对脂多糖所致大鼠急性肺损伤(ALI)的干预作用,明确芪冬活血饮的保护作用并探讨其作用机制。方法:将50只SD大鼠随机分为空白组,模型组,高、中、低剂量中药治疗组5组。气道内滴注脂多糖建立急性肺损伤模型。中药治疗组以芪冬活血饮灌胃,空白组及模型组以0.9%氯化钠溶液灌胃。各组大鼠造模后24 h处死,收集标本。结果:1芪冬活血饮可以减轻肺损伤大鼠肺泡结构破坏,肺水肿及炎性细胞浸润。2ALI大鼠肺泡灌洗液肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1β、IL-10水平增高,芪冬活血饮降低TNF-α、IL-1β水平,升高IL-10水平,高剂量组与低剂量组比较差异有统计学意义(P<0.01)。3ALI大鼠Toll样受体-4(TLR4)、核转录因子-κB(NF-κB)p65蛋白及m RNA表达增加,芪冬活血饮可减少TLR4、NF-κB p65蛋白及m RNA表达,并有一定的剂量相关性。结论:芪冬活血饮对LPS诱导的大鼠ALI有保护作用,其机制与抑制TLR4/NF-κB p65炎症信号通路,降低促炎细胞因子TNF-α、IL-1β水平,升高抗炎细胞因子IL-10水平有关。Objective： To investigate the protective effect of qidonghuoxue decoction（QD） on acute lung injury（ALI） in rats induced by lipopolysaccharide（LPS）, and to explore the mechanism. Methods： Fifty SD rats were divided into five groups randomly： control group, model group, high-dose QD group, medium-dose QD group, low-dose QD group. The ALI model was established by intratracheal instillation of LPS. QD was administrated via esophagus to rats in QD groups; NS was substitution in control and model groups. All rats were executed 24 h after modeling, bronchoalveolar lavage fluid（BALF） and lung tissue were collected. Results： 1HE staining showed that QD could reduce alveolar damage, pulmonary edema and inflammatory cells infiltration in rats with ALI. 2TNF-α, IL-1β, IL-10 levels were increased in rats with ALI, QD decreased the levels of TNF-α and IL-1β, increased the level of IL-10, there was significant difference between the high-dose and lowdose group（P〈0.01）. 3The protein and m RNA expression of TLR4/NF-κB p65 both increased in rats with ALI, while QD reduced the expression,and the effect was kind of dose-related. Conclusion： QD has a protective effect on ALI induced by LPS in rats, its mechanism is related to inhibit TLR4/NF-k B p65 signaling pathway, decrease IL-1β/TNF-α levels and increase IL-10 level.

关 键 词：急性肺损伤 TOLL样受体-4 核转录因子ΚB 细胞因子 

分 类 号：R363[医药卫生—病理学]