通心络超微粉对“络气虚滞”大鼠血管氧化损伤的保护作用  

Protective Effect of Tongxinluo Superfine Powder on Oxidative Injury in Rats with Qi Deficiency and Blood-Stasis Blocking Collaterals

作　　者：袁凌燕[1,2] 张红旗[3] 徐丹令[1] 王克强[1] 邹云增[1] 贾剑国[1] 李冰玉[1] 孙爱军[1] 郝颖[1] 葛均波[1] 

机构地区：[1]复旦大学附属中山医院心血管病研究所,上海市枫林路180号200032 [2]上海师范大学体育学院 [3]复旦大学上海医学院

出　　处：《中医杂志》2009年第7期642-645,共4页Journal of Traditional Chinese Medicine

基　　金：国家重点基础研究发展计划("973"计划)资助项目(2005CB523302;2006CB503803)

摘　　要：目的从烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化损伤途径,探讨通心络超微粉保护络脉"络气虚滞"大鼠血管内皮的作用机制。方法选用8周龄SD大鼠,采用力竭性跑台运动,并结合基础饮食建立气虚证候模型,同时采用200ng.min-1.kg-1血管紧张素Ⅱ(AngⅡ)建立大鼠脉络"络气虚滞"的病理证候复合模型,随机分成正常组、模型组和通心络组,每组10只。14天后测定血内皮素(ET)、一氧化氮(NO)、AngⅡ、白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α),主动脉内皮形态结构及主动脉内皮核转录因子kappaB(NF-κB)、血管细胞黏附分子1(VCAM-1)、内皮一氧化氮合酶(eNOS)的表达。结果模型组大鼠内皮见内皮细胞成片脱落,通心络组血管内皮仅有轻微的损伤;模型组血ET、IL-6、TNF-α增加(P<0.05或P<0.01),NO降低(P<0.05),通心络可以增加血清NO含量,降低血ET、IL-6、TNF-α(P<0.05);模型组p22phoxmRNA(P<0.01)、NF-κB、VCAM-1表达增加,eNOS表达降低,通心络可不同程度地逆转上述变化。结论通心络通过减少血管NADPH—氧化—炎症损伤途径,减轻血管内皮损伤。Objective To investigate the mechanism of Tongxinluo Superfine Powder（Powder for removing obstruction of collaterals） in protecting the endothelium by observing the endothelium oxidative injury caused by nicotinamide adenine dinucleotide phosphate（NADPH） in rats with qi deficiency and blood-stasis blocking collaterals.Methods The animal model of ＂qi deficiency and blood-stasis blocking collaterals＂ was induced by starvation and exhaustion exercise in 8-week-old SD rats and endothelium injury was established by angiotensin Ⅱ infusion at a rate of 200ng/kg per min. The SD rats were randomly divided into 3 groups： control group, model group and Tongxinluo group with 10 in each. After treatment of 14 days, the content of endothelin （ET）, nitric oxide （NO）, angiotensin Ⅱ （Ang Ⅱ ）, interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α）, morphology of endothelial cells in the thoracic aorta, and the nuclear kappa B （NF-κB）, vascular cell adhesion molecule-1 （VCAM-1） and endothelial nitric oxide synthase （eNOS） expression in aorta were observed. Results In the model group, there existed the massive cell detachments in vascular endothlium, while in Tongxinluo group, only a mild injury was observed. The blood ET, IL-6 and TNF-α increased （P〈0.05 or P〈0.01）, NO decreased （P〈0.05） in the model group, while in Tongxinluo group, the result was opposite. The p22phox mRNA （P〈0.01）, NF- κB, and VCAM-1 expression increased significantly in the model group, moreover, eNOS expression decreased. These changes in Tongxinluo group were reversed to different degrees. Conclusion Tongxinluo protects endothelium by inhibiting NADPH - oxidation - inflammatory injury of vessels in rats with qi deficiency and blood-stasis blocking collaterals.

关 键 词：通心络超微粉 血管紧张素 内皮损伤 氧化应激 络气虚滞 

分 类 号：R285.5[医药卫生—中药学]