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目的探讨葛根素对糖尿病大鼠心肌的保护作用,并探讨其作用机制。方法一次性腹腔注射链脲佐菌素(STZ)诱导雄性SD大鼠。取造模成功的大鼠40只,随机分成四组:模型组、葛根素低剂量组(40mg/kg)、葛根素中剂量组(80mg/kg)、葛根素高剂量组(160mg/kg),每组10只。另取同龄正常饲养大鼠10只作为对照组。按组别给予不同药物干预12周后分别测定大鼠血清Ang-Ⅱ水平,测定舒张末期室间隔厚度(IVSTd)、舒张末期左心室后壁厚度(LVPWTd)、左室舒张末期内径(LVEDd)、收缩末期左心室内径(LVEDs)及左室射血分数(LVEF),HE染色观察心肌组织病理学改变。结果与模型组比较,葛根素各组大鼠Ang-Ⅱ水平下降,以葛根素高剂量组下降最明显(P<0.05);与模型组相比,葛根素各组IVSTd、LVPWTd、LVEDd及LVEDs降低,其中以葛根素高剂量组变化更为明显(P<0.05);葛根素高剂量组心肌组织结构紊乱程度减轻,纤维组织增生减轻,中性粒细胞聚集减少。结论葛根素可抑制肾素血管紧张素系统,并通过此机制对心脏起保护作用。
Objective To investigate the protective effect of puerarin on myocardium of diabetic rats and its mechanism. Methods Male SD rats were induced by intraperitoneal injection of streptozotocin (STZ). Forty rats were randomly divided into four groups: model group, low dose of puerarin (40mg / kg), middle dose of puerarin (80mg / kg), high dose of puerarin (160mg / kg) , Each group of 10. Another normal age rats fed another 10 as a control group. The serum levels of Ang-Ⅱ in rats were measured after 12 weeks of intervention by different groups. The left ventricular posterior wall thickness (IVSTd), left ventricular posterior wall thickness (LVPWTd), left ventricular end-diastolic diameter (LVEDd) Left ventricular end-diastolic dimension (LVEDs) and left ventricular ejection fraction (LVEF) were observed at the end of systole. Pathological changes of myocardium were observed by HE staining. Results Compared with the model group, the levels of Ang-Ⅱ in Puerarin decreased significantly in the Puerarin high dose group (P <0.05). Compared with the model group, the levels of IVSTd, LVPWTd, LVEDd and LVEDs (P <0.05). In the high-dose puerarin group, the disturbance of myocardial tissue structure was alleviated, the proliferation of fibrous tissue was reduced, and the neutrophil aggregation was reduced. Conclusion Puerarin inhibits the renin-angiotensin system and protects the heart through this mechanism.