首页> 中文期刊> 《中西医结合心脑血管病杂志 》 >补肾活血汤对慢性心力衰竭大鼠心功能及免疫炎症反应的影响

补肾活血汤对慢性心力衰竭大鼠心功能及免疫炎症反应的影响

             

摘要

目的 观察补肾活血汤对慢性心力衰竭大鼠心功能以及血清白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、血清正五聚蛋白3(PTX3)水平的影响,并探讨其治疗心力衰竭的潜在作用机制.方法 通过腹腔注射阿霉素复制心力衰竭模型,将造模成功后的Wistar大鼠随机分为补肾活血汤高剂量组、补肾活血汤中剂量组、补肾活血汤低剂量组、卡托普利组、模型组,并设立空白组,分别给药4周,空白组灌胃生理盐水4周.利用心脏彩超测量左心室射血分数(LVEF)、左室短轴缩短率(LVFS).用酶联免疫法(ELISA)检测心力衰竭大鼠血清中IL-6、TNF-α、PTX3及脑钠肽(BNP)水平.结果 与空白组相比,模型组LVEF、LVFS水平明显降低(P <0.01);与模型组相比,补肾活血汤中剂量组和高剂量组LVEF、LVFS水平明显升高(P <0.05或P <0.01),IL-6、TNF-α、PTX3及BNP水平明显下降(P <0.01).结论 补肾活血汤能调控心力衰竭时大鼠细胞因子及神经内分泌水平,这可能是补肾活血汤减少心力衰竭炎症细胞因子分泌、改善神经内分泌紊乱、干预心室重构、抑制心力衰竭的生化机制之一.%Objective To observe the effect of Bushen Huoxue decoction (BHD) on cardiac function and the levels of serum interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and serum pentameric protein 3 (PTX3) in rats with chronic heart failure (CHF), and to explore its potential mechanism.Methods The rat model of CHF was established by intraperitoneal injection of doxorubicin.After successful modeling, Wistar rats were randomly divided into BHD high-dose group, BHD medium-dose group, BHD low-dose group, captopril group and model group, and a blank group was set up.After 4 weeks of administration, the rats in blank group were orally administered with normal saline for 4 weeks.The left ventricle ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were calculated by color Doppler echocardiography to evaluate cardiac function.The levels of serum IL-6, TNF-α, PTX3 and brain natriuretic peptide (BNP) were detected by enzyme-linked immunosorbent assay (ELISA).Results Compared with the blank group, the levels of LVEF and LVFS in the model group were significantly lower (P <0.01).Compared with the model group, the levels of LVEF and LVFS in BHD medium-dose group and BHD high-dose group were significantly increased (P <0.05 or P <0.01), IL-6, TNF-α, PTX3 and BNP levels were significantly decreased (P <0.01).Conclusion BHD can regulate the levels of cytokines and neuroendocrine in rats with CHF.This may be one of the biochemical mechanisms of BHD to reduce the secretion of inflammatory cytokines, improve neuroendocrine disorders, interfere with ventricular remodeling, and inhibit heart failure.

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