失血性休克小鼠心肌Toll样受体2/4 mRNA的表达  

Expression of Toll-like receptor 2/4 mRNA in myocardium in mice with hemorrhagic shock

作　　者：杭涛[1] 江时森[1] 宫剑滨[1] 吕镗锋[2] 宋勇[2] 诸葛海鸿[1] 

机构地区：[1]南京军区南京总医院心脏内科,江苏南京210002 [2]南京军区南京总医院呼吸内科,江苏南京210002

出　　处：《中国危重病急救医学》2006年第9期554-557,共4页Chinese Critical Care Medicine

摘　　要：目的探讨无复苏对失血性休克小鼠心肌Toll样受体(TLR)表达变化的影响及其意义。方法将45只C57BL/6小鼠随机分为失血性休克模型组、假手术组、脂多糖(LPS)组(由尾静脉注射LPS5mg/kg),每组15只;采用心脏穿刺法建立小鼠失血性休克模型。心肌TLR2mRNA和TLR4mRNA表达采用逆转录聚合酶链反应(RT PCR)方法进行分析;测定左室收缩末压(LVESP)以反映左室收缩功能。结果1与假手术组比较,失血性休克及LPS刺激后小鼠的动脉血压出现下降,均可导致左室收缩功能障碍;2失血性休克及LPS刺激后TLR2和TLR4的mRNA表达水平均出现不同程度上调,而假手术组在各时间点未见明显改变。结论1失血性休克及LPS刺激后心肌TLR2及TLR4的mRNA表达上调与心功能障碍存在密切联系,但这两种病理状态下的信号转导通路可能存在差异;2失血性休克和LPS刺激后TLR2、TLR4的mRNA升高增强了机体的天然免疫功能,提高了机体对急性炎症的应激能力,对机体具有保护作用,但其过度表达也可能对组织、器官功能产生损害。Objective To investigate the effect of hemorrhagic shock without resuscitation on expression of Toll-like receptor （TLR） in myocardium of rats and its significance. Methods Forty-five C57BL/6 mice were randomly divided into 3 groups： hemorrhagic group, sham operation group and lipopolysaccharide （LPS） group, with 15 mice in each group. The hemorrhagic shock mouse model was reproduced by heart puncture. Expression levels of TLR2 mRNA and TLR4 mRNA were determined by reverse transcription- polymerase chain reaction （RT- PCR）. Left ventricular end-systolic pressure （LVESP） was determined and adopted as an index of left ventricle contractile function. Results ①Both hemorrhagic shock and LPS challenge led to a reduction in arterial blood pressure in mice when compared with sham operation group. Both hemorrhagic shock and LPS challenge could result in left ventricle contractile dysfunction when compared with sham operation group. ②Expression levels for TLR2 and TLR4 genes were upregulated in myocardium to various extents after hemorrhagic shock and LPS challenge, while in contrast the changes were absent in sham operation group. Conclusion ①The up-regulation of TLR2 and TLR4 genes is closely related with hemorrhagic shock and LPS-induced left ventricle contractile dysfunction, and there may exist a difference in signal transduction pathway between the two pathological conditions. ②The host ability of innate immune response may be reinforced by the up-regulation of TLR2 and TLR4, whereas overexpression of them may also impair the function of tissues or organs.

关 键 词：TOLL样受体 心肌 休克 失血性 脂多糖 小鼠 

分 类 号：R459.7[医药卫生—急诊医学]