“失血加LPS”大鼠肺脏IκBα和TLR4基因表达及参麦的肺脏保护作用

被引:14
作者
袁兆新 [1 ]
刘潇 [1 ]
季东平 [1 ]
张旭 [2 ]
王志 [1 ]
李扬 [1 ]
赵雪俭 [1 ]
孙连坤 [1 ]
机构
[1] 吉林大学基础医学院病理生理教研室
[2] 长春医学高等专科学校
关键词
中草药; 地塞米松; 脂多糖类; 受体,Toll样; 核因子-κB抑制蛋白α; 肿瘤坏死因子;
D O I
暂无
中图分类号
R363 [病理生理学];
学科分类号
摘要
目的:探讨参麦注射液的抗休克效果及其作用机制。方法:大鼠随机分为单纯失血性休克(HS)组、失血加脂多糖(HS+LPS)组、地塞米松(HS+LPS+Dex)组和参麦注射液(HS+LPS+SM)组。HS+LPS组大鼠模型复制:首先,大鼠放血至MAP40mmHg,维持10min(失血性休克),然后舌下静脉注射LPS(1·5mg/kg)。4h后留取肺脏组织,RT-PCR法测定IκBα和TLR4mRNA表达、ELISA法测TNF-α含量,并进行肺脏组织电镜观察。结果:HS+LPS+SM组TLR4mRNA表达明显低于HS+LPS组(P<0·05);HS+LPS+SM组IκBαmRNA表达明显高于HS+LPS组(P<0·05);HS+LPS+SM组肺脏组织匀浆TNF-α含量明显低于HS+LPS组(P<0·05);HS+LPS+SM组肺组织病理损伤显著轻于HS+LPS组。结论:参麦注射液能够下调肺脏组织中TLR4mRNA表达,同时上调IκBα的表达,进而抑制促炎介质TNF-α释放,提示参麦注射液可能通过调节NF-κB信号转导途径抑制炎症反应而对机体细胞起保护作用。
引用
收藏
页码:730 / 733
页数:4
相关论文
共 7 条
[1]  
Suppression of inducible cyclooxygenase andinducible nitric oxide synthase by apigenin and relatedflavonoids in mouse macrophages. Liang YC,Tsai SH,Tsai DC,et al. Carcinoma-genesis . 1999
[2]  
Murine Toll like receptor4confers lipopolysaccharide responsiveness as determined by activation of NF kappa B and expression of the inducible. Rhee SH,Hwang D. Journal of Biological Chemistry . 2000
[3]  
Toll-like re-ceptor-4mediates lipopolysaccharide-induced signal trans-duction. ChowJC,Young DW,Golenbock DT,et al. Journal of Biological Chemistry . 1999
[4]  
Suppression of NF-κB ac-tivation and cytokine production by N-acetylcysteine in pan-creatic acinar cells. Kim H,Seo JY,Roh KH,et al. Free Radical Biology and Medicine . 2000
[5]  
ACBPintegrator complex mediates transcriptional activation and AP-1inhibition by nu-clear receptors. Kamei Y,Xu L,Heinzel T,et al. Cell . 1996
[6]  
Induction of IκBαmRNAex-pressionin the brain by glucocorticoids:Anegative feedback mechanismfor immune-to-brain signaling. Quan N,He L,Lai W,et al. The Journal of Neuroscience . 2000
[7]  
Protective effects of apoc-ynin on"two-hit"injury induced by hemorrhagic shock and lipopolysaccharide. Zhou R,Hu DY,Liu LM,et al. J Acta Pharmacol Sin . 2002