基于络脉理论从AMPK-SIRT1-NK-kB信号途径研究灸法抗血管内皮细胞损伤防治动脉粥样硬化形成机制

项目名称： 基于络脉理论从AMPK-SIRT1-NK-kB信号途径研究灸法抗血管内皮细胞损伤防治动脉粥样硬化形成机制

项目编号： No.81460703

项目类型： 地区科学基金项目

立项/批准年度： 2015

项目学科： 医药、卫生

项目作者： 杨孝芳

作者单位： 贵州中医药大学

项目金额： 50万元

中文摘要： 研究揭示络脉与血管在结构和功能上密切相关，而痰瘀毒阻络是心血管病重要机制，由此从络论治至关重要。动脉粥样硬化(AS)是心血管疾病的关键环节，其中血管内皮细胞损伤是AS病变的始动因素，沉默因子（SIRT1）信号途径在血管内皮细胞损伤中起重要调控作用。前期研究表明灸法适宜温热刺激能增强络脉相关血管内皮细胞的AMP激活的蛋白激酶（AMPK）的活性，促进SIRT1分泌达到通络行血、抗衰老等生物学效应。本项目抓住抑制血管内皮损伤抗AS形成机制，以AS模型家兔为研究对象，神阙灸为刺激方法，用小动物活体成像技术从整体层面探明灸法治疗AS的刺激于外，调节于内的整体作用效应和靶点；使用免疫组化、FQ-PCR）和Western blotting等生物学技术手段从AMPK-SIRT1- NF-κB信号途径研究灸法抑血管内皮损伤抗AS形成机制，为丰富络脉理论和深化灸法防治AS提供新的思路。

中文关键词： 灸法；温热刺激；动脉粥样硬化；血管内皮细胞损伤；沉默因子

英文摘要： researches have revealed that collaterals have close relationship with the structures and functions of blood vessel, also phlegm, stagnation and toxin are the significant mechanism and critical link of cardiovascular diseases. Therefore, treating cardiovascular diseases from collaterals is very crucial. Atherosclerosis (AS) is the important pathological basis and critical link of cardiovascular diseases. Vascular endothelial cell damage is the initial factors of AS, while the silent information regulator 1 (SIRT1) signal pathway plays vital regulating effects in vascular endothelial damage. Previous studies indicate that moxibustion at suitable thermal stimulation can enhance activity of AMP-activated protein kinase (AMPK) in the vascular endothelial cells which relate to collaterals, facilitate secretion of SIRT1 to achieve the biological effects of dredging collaterals, promoting circulation of blood and anti-aging. This project catches hold of the anti-atherosclerosis formation mechanism in AS researches about inhibiting vascular endothelial injury, in the project AS model rabbit as research object and moxibustion on Shenque (CV8) as stimulating method. Then we are going to ascertain the entire action effect and target spot of moxibustion that treat AS at the integral level through small animal living imaging, which based on stimulation outside to generate regulation inside. Finally, we will apply biological technological means to study the mechanism how moxibustion inhibit vascular endothelial damage to realize anti-atherosclerosis from signal pathway of AMPK-SIRT1- NF-κB, including immunohistochemical, FQ-PCR and Western blotting. We hope this project can provide some novel thinking to enrich the collateral theory and intensify preventing and treating AS with moxibustion.

英文关键词： moxibustion;thermal stimulation;atherosclerosis;vascular endothelial cell damage;silent information regulator 1