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目的:初步探讨芪苈强心胶囊对阿霉素致心肌病大鼠心功能及血清因子的影响及其机制。方法:将29只SD大鼠中9只作为正常对照组,20只用作造模。造模大鼠2周内分6次腹腔注射阿霉素2.5mg/kg作为心力衰竭(心衰)模型后,分为心衰组、芪苈强心组和美托洛尔组,后2组分别服用芪苈强心胶囊生粉(1g/kg)和美托洛尔(10mg/kg)治疗6周,正常对照组和心衰组以相同体积0.9%氯化钠溶液灌胃6周。超声心动图检测各组大鼠心功能指标,ELISA法检测大鼠血清肿瘤坏死因子-α(TNF-α)和B型钠尿肽(BNP)含量,心肌组织苏木素-伊红染色病理检验。结果:心衰组较正常对照组心功能显著降低,左心室收缩末期内径(LVESD)和左心室舒张末期内径(LVEDD)显著增加(P<0.01和P<0.05),左室射血分数(LVEF)和短轴缩短率(FS)显著降低(均P<0.01),血清BNP和TNF-α水平明显升高(均P<0.01)。美托洛尔组较心衰组显著改善了大鼠的LVESD、LVEDD、LVEF和FS(均P<0.05),BNP显著低于心衰组(P<0.05)。芪苈强心组较心衰组也改善了大鼠LVEF和FS(均P<0.05),显著降低心衰大鼠血清TNF-α水平(P<0.01)。芪苈强心组与美托洛尔组心功能比较,差异无统计学意义(P>0.05),BNP和TNF-α均差异有统计学意义(P<0.05和P<0.01)。病理切片经染色发现:心衰组心肌存在心肌部分坏死;美托洛尔组心肌纤维间有大量炎症细胞浸润,炎症周围的心肌纤维排列尚规则,横纹可见;芪苈强心组心肌纤维排列尚规则,横纹可见,心肌纤维间少量炎细胞浸润。结论:芪苈强心胶囊有改善心功能、降低血清炎性因子TNF-α水平及减轻心肌纤维炎症细胞浸润的作用。
Objective: To investigate the effect and mechanism of Qili Qiangxin capsule on cardiac function and serum factor in rats with adrimycin-induced cardiomyopathy. Methods: Nine of 29 Sprague-Dawley rats were used as normal control group and 20 as model control. The model rats were divided into heart failure group, Qiliqiangxin group and metoprolol group by intraperitoneal injection of doxorubicin 2.5mg / kg intraperitoneally 6 times within 2 weeks The patients in the control group and the heart failure group were given gavage with 0.9% sodium chloride solution of the same volume for 6 weeks after taking Qiliqiangxin capsule powder (1g / kg) and metoprolol (10mg / kg) for 6 weeks. The cardiac function indexes of rats in each group were detected by echocardiography. The contents of tumor necrosis factor-α (TNF-α) and B-type natriuretic peptide (BNP) in serum were detected by ELISA, and the hematoxylin- Results: Compared with the normal control group, the heart function of the heart failure group was significantly decreased, the LVESD and LVEDD were significantly increased (P <0.01 and P <0.05) (P <0.01), serum BNP and TNF-α levels were significantly increased (all P <0.01). Metoprolol group significantly improved LVESD, LVEDD, LVEF and FS (all P <0.05), BNP was significantly lower than that of heart failure group (P <0.05). Qiliqiangxin group also improved LVEF and FS (all P <0.05), and significantly decreased the level of serum TNF-α in heart failure rats (P <0.01). There was no significant difference in cardiac function between Qiliqiangxin group and metoprolol group (P> 0.05). There was significant difference between BNP and TNF-α (P <0.05 and P <0.01). The pathological sections were stained and found that there was myocardial necrosis in the heart of the heart failure group. There was a large number of infiltration of inflammatory cells in the myocardium of the metoprolol group. The arrangement of myocardial fibers around the inflammation was regular and the stripes were visible. Still rules, stripes can be seen, a small amount of infiltration of myocardial cells between inflammatory cells. Conclusion: Qili Qiangxin capsule can improve cardiac function, decrease the level of serum inflammatory cytokines TNF-α and reduce the infiltration of myocardial fibrosis cells.