山莨菪碱对兔失血性休克合并内毒素血症诱发肝脏损伤的保护机制研究  

Protective Role of Anisodamine Against Rabbit Liver Injury by Hemorrhage Shock Complicated with Endotoxemia and the Underlying Mechanism

作　　者：刘健[1] 尹文[1] 袁顺书[1] 宋祖军[1] 袁军[1] 虎晓岷[1] 张松涛[1] 张永和[1] 

机构地区：[1]第四军医大学西京医院急诊科,陕西西安710032

出　　处：《中国医师杂志》2005年第9期1153-1155,共3页Journal of Chinese Physician

基　　金：国家自然科学基金资助项目(30000165)

摘　　要：目的研究山莨菪碱(654-2)对失血性休克合并内毒素诱发肝脏损伤可能的保护机制。方法通过失血性休克和内毒素双向打击制备家兔休克模型,采用原位杂交法(ISH)结合原位定量分析检测肝枯否细胞(KC)中HSP70和NF-κB的mRNA表达,并进行肝脏组织的病理学光镜检查。结果休克组KC中HSP70mRNA的表达为(0.1565±0.0260),NF-κBmRNA表达为(0.1659±0.0103),均较正常对照组HSP70mRNA和NF-κBmRNA的表达[分别为(0.0328±0.0201)(0.0256±0.0043)]显著增高(P<0.01)。654-2能明显提高休克动物KC中HSP70的表达(0.2019±0.0396)同时能显著抑制NF-κBmRNA的表达(0.1276±0.0083)(P<0.01),并能缓解肝脏的损伤程度。结论654-2可能通过激活HSP70的表达,从而抑制NF-κB的活性发挥对失血性休克继发肝脏损害的保护作用。Objective To study the possible protective mechanisms of Anisodamine against liver injury induced by hemorrhage shock（HS）. Methods In this study, we established animal models induced by HS and endotoxin, observed the expressions of NF-κB mRNA and heat shock protein 70（HSP 70） mRNA by In-situ hybridization （ISH） in liver kupffercells（KC） and studied the pathologic changes of the liver tissue by microscope. Results After stimulus of HS and injection of endotoxin, the mRNA expressions of HSP70 and NF-κB in KC were （0.1565±0.0260） and （0.1659±0.0103）, respectively, and significantly higher than those in the control group （0.0328±0.0201; 0.0256±0.0043） （P〈0.01）, Anisodamine could significantly enhance the expression of HSP70mRNA （0.2019±0.0396）, suppress the expression of NF-κB mRNA （0.1276±0.0083） （P〈0.01）, and alleviate the damage of liver tissue. Conclusion By enhancing the expression of HSP70, anisodamine suppresses the activation of NF-κB and therefore plays a protective role against the liver injury induced by HS.

关 键 词：山莨菪碱 休克 失血性:肝损伤 热休克蛋白质类70 核因子-κB 失血性休克 内毒素血症 肝脏损伤 保护机制 HSP70MRNA 机制研究 

分 类 号：R96[医药卫生—药理学]