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目的探讨黄芪对阿霉素诱导扩张型心肌病(DCM)大鼠的干预作用。方法采用腹腔注射阿霉素成功建立SD大鼠DCM模型后分别实施培哚普利3mg·kg~(-1)·d~(-1)(A组,13只),美托洛尔50mg/kg(B组,12只),黄芪3.5mg·kg~(-1)·d~(-1)(D组,13只)或等体积蒸馏水(E组,10只)干预,连续灌胃给药8周。另取20只SD大鼠作为空白对照(C)组。检测指标:心脏超声检查,ELISA法测定大鼠血清脑钠肽(BNP)水平,取大鼠左心室心肌行HE染色,RT-PCR法测定心肌组织Bax、Bcl-2、FasL、Fas、Caspase-3 mRNA水平;C、D、E组行心肌代谢显像检查。结果与E组比较,A、B、D组大鼠左心室舒张末期内径、左心室收缩末期内径及血清BNP下降(P<0.01),左心室射血分数和短轴缩短率升高(P<0.01)。HE染色示A、B、D组大鼠心肌纤维化程度有改善。与E组比较,A、B、D组Bax、FasL、Fas、Caspase-3 mRNA表达下降,而Bcl-2 mRNA表达升高(P<0.05或P<0.01),D组大鼠最大标准化摄取值升高(5.97±0.53vs.1.04±0.28)(P<0.01)。结论黄芪能改善心肌活性。其作用机制可能与调节心肌细胞凋亡的线粒体途径和/或死亡受体途径相关因子表达相关。
Objective To investigate the intervention of astragalus on doxorubicin-induced dilated cardiomyopathy (DCM) in rats. Methods SD rat models of DCM were established by intraperitoneal injection of doxorubicin. Perindopril 3 mg · kg -1 · d -1 (group A, n = 13), metoprolol 50 mg / (group B, n = 12), Astragalus (3.5 mg · kg -1 · d -1) (group D, n = 13) or equal volume of distilled water Medicine for 8 weeks. Another 20 SD rats as blank control (C) group. The levels of Bax, Bcl-2, FasL, Fas and Caspase-3 in myocardium were measured by RT-PCR. 3 mRNA levels; C, D, E group myocardial metabolic imaging examination. Results Compared with group E, left ventricular end-diastolic dimension, left ventricular end-systolic diameter, and serum BNP decreased in group A, B and D (P <0.01), left ventricular ejection fraction and short axis shortening increased (P < 0.01). HE staining showed that the degree of myocardial fibrosis in groups A, B and D was improved. Compared with group E, the expression of Bax, FasL, Fas, Caspase-3 mRNA decreased and the expression of Bcl-2 mRNA increased in group A, B and D (P <0.05 or P <0.01) (5.97 ± 0.53vs.1.04 ± 0.28) (P <0.01). Conclusion Astragalus can improve myocardial activity. Its mechanism of action may be related to the mitochondrial pathway and / or death receptor pathway related factor expression regulating cardiomyocyte apoptosis.