益气活血解毒方对幼龄自发性高血压大鼠内皮功能的影响

Effect of Formula of Benefiting Qi and Promoting Blood Circulation and Detoxication on Endothelial Function in Younger Spontaneously Hypertensive Rats

摘要:

目的 :研究益气活血解毒方对幼龄自发性高血压大鼠内皮功能的影响,探讨益气活血解毒方预防高血压病的机制。 方法 :雄性6周幼龄自发性高血压大鼠(SHR)16只随机分为益气活血解毒方组、模型组,治疗6周,分别检测治疗前后的各组大鼠血压,酶联免疫吸附(ELISA)法测定血清血管性假血友病因子(vWF)、内皮素-1(ET-1),硝酸还原法测定一氧化氮(NO)的含量,黄嘌呤及黄嘌呤氧化酶反应系统检测超氧化物歧化酶(SOD),硫代巴比妥酸比色法检测丙二醛 (MDA)。并设同龄Wistar-Kyoto(WKY)大鼠8只做空白对照比较。 结果 :幼龄SHR血浆中vWF和MDA升高,NO和SOD降低,益气活血解毒方可以降低幼龄SHR血浆vWF和MDA,升高NO和SOD。 结论 :幼龄SHR已存在内皮功能不全,益气活血解毒方早期应用能改善SHR血管内皮功能。

Abstract:

Objective: To study the influence of the formula of benefiting Qi and promoting blood circulation and detoxication on juvenile spontaneously hypertensive rats(SHR)’ endothelium function, and further investigate the prevention mechanism of HBP by the formula. Method: 16 6ws-old male SHR rats were randomly divided into two groups, including the model group and the formula group. After 6 weeks, the changes in blood pressure before and after treatment were detected separately. Besides, the change of serum von Wilebrand factore(vWF) and ET-1 concentration were tested by enzyme linked immunosorbent assay, the content of serum NO was tested by nitrous reductase chromatometry, the SOD was tested by xathine and xanthylic oxidase reaction system, and the MDA was tested by thiobarbital chromatometry. Meanwhile 8 same age WKY rats were used as the blank comparison. Results : In the juvenile plasma, vWF and MDA were significantly (P<0.05) increased, NO and SOD were significantly (P<0.05) decreased. After treatment with the formula of benefiting Qi and promoting blood circulation and detoxication, not only vWF and MDA were significantly (P<0.05) decreased, but also NO and SOD were significantly (P<0.05) increased in the SHP plasma. Conclusion : The insufficiency of endothelium in SHR exists in juvenile stage. The early application with the formula of benefiting Qi and promoting blood circulation and detoxication can improve vascular endothelial function in juvenile SHR.