复方血栓通胶囊对弥散性血管内凝血模型大鼠炎症抑制作用及机制研究  

Mechanism and anti-inflammatory effect of compound Xueshuantong capsules on rats with disseminated intravascular coagulation

作　　者：刘宏[1,2] 生书晶 李沛波 张伟健[1] 陈滔彬 彭维 姚宏亮[1] 苏薇薇[1] LIU Hong;SHENG Shu-jing;LI Pei-bo;ZHANG Wei-jian;CHEN Tao-bin;PENG Wei;YAO Hong-liang;SU Wei-wei(School of Life Sciences,Sun Yat-sen University,Guangdong Engineering and Technology ResearchCenter for Quality and Efficacy Re evaluation of Post-marketed TCML Guangdong Key Laboratory of Plant Resources,Guangzhou 510215;Guangdong Zhongsheng Pharmaceutical Co.,Ltd.,Dongguan Guangdong 523325)

机构地区：[1]中山大学生命科学学院,广东省中药上市后质量与药效再评价工程技术研究中心,广东省热带亚热带植物资源与利用重点实验室,广州510275 [2]广东众生药业股份有限公司,广东东莞523325

出　　处：《中南药学》2019年第10期1617-1621,共5页Central South Pharmacy

基　　金：中国博士后科学基金特别资助（No.2018T110857）;中国博士后科学基金面上项目（No.2018M643036）;广东省名优中成药二次开发项目（粤中医函2017-No.19）

摘　　要：目的研究复方血栓通胶囊对弥散性血管内凝血(DIC)模型大鼠血管内皮功能调节及炎症抑制的作用,并揭示其抑制炎症反应的作用机制。方法采用尾静脉注射脂多糖(LPS)诱导DIC大鼠模型,考察药物处理对模型大鼠体内内皮素-1(ET-1)、一氧化氮(NO)浓度及诱导型一氧化氮合酶(i NOS)活力的影响;考察药物处理对模型大鼠体内肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)、白介素-8(IL-8)、高敏C反应蛋白(hs-CRP)、人单核细胞趋化蛋白-1(MCP-1)浓度的影响,研究其与炎症相关NF-κB信号转导通路的关系。结果 DIC模型大鼠体内NO、ET-1浓度均显著提高,NO/ET-1比值显著降低,即LPS导致了血管内皮损伤。复方血栓通胶囊能够显著改善模型大鼠体内NO/ET-1,其机制与抑制i NOS活力相关;能够显著抑制模型大鼠体内TNF-α、IL-1β、IL-6、IL-8、MCP-1升高,其机制与抑制IκB-α的降解及p65的入核,即抑制NF-κB激活相关。结论复方血栓通胶囊能够改善血管内皮功能、抑制炎症反应,为进一步弄清其抗血栓、保护心血管的作用机制提供了依据。Objective To determine the mechanism and effect of compound Xueshuantong capsules(CXC) on the vascular endothelial function and inflammatory response in rats with disseminated intravascular coagulation(DIC). Methods Rats were injected LPS through the tail vein to induce the DIC model. After the CXC treatment, concentrations of ET-1 and NO and iNOS activity were detected. Effect of drugs on the concentrations of TNF-α, IL-1β, IL-6, IL-8, hs-CRP and MCP-1, and inflammation related NF-κB pathway were detected. Results ET-1 and NO concentrations were increased while NO/ET-1 decreased significantly in the DIC rats, suggesting LPS-induced vascular endothelial injury. CXC regulated the NO/ET-1 obviously by inhibiting iNOS activity. CXC inhibited the increase in TNF-α, IL-1β, IL-6, IL-8, and MCP-1 significantly, which was related to the suppression of IκB-α degradation and p65 nuclear translocation, thus inhibiting the NF-κB pathway activation. Conclusion CXCs help improve the vascular endothelial function and suppress the inflammation response, contributing to understanding anti-thrombus and cardiovascular protection of the mechanism of CXC.

关 键 词：复方血栓通胶囊 弥散性血管内凝血 炎症 作用机制 

分 类 号：R286[医药卫生—中药学]