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作 者:苗梦露[1] 李七一[2] 严士海[3] 朱波[2] 戴海云[1]
机构地区:[1]南京中医药大学研究生院,南京医学博士研究生210046 [2]江苏省中医院心内科,南京210029 [3]江苏省中医院临床药理科,南京210029
出 处:《医学研究生学报》2013年第9期937-940,共4页Journal of Medical Postgraduates
摘 要:目的心肌纤维化是舒张性心力衰竭(diastolic heart failure,DHF)的重要机制,文中观察抗心力衰竭颗粒对DHF大鼠心肌肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)及胶原表达的影响,以探讨其对心肌纤维化的作用及治疗DHF的机制。方法用腹主动脉缩窄法的方法建立压力超负荷型舒张性心力衰竭大鼠模型,按完全随机分组法分为分为模型组,贝那普利组,抗心力衰竭颗粒大、中、小剂量组和假手术组,用Western blot法检测其心肌TNF-α及Ⅰ型胶原、Ⅲ型胶原的表达,并以Masson染色观察胶原沉积。结果模型组大鼠心肌TNF-α及Ⅰ型胶原、Ⅲ型胶原均较假手术组明显增多,差异有统计学意义(P<0.01),贝那普利组及抗心力衰竭颗粒大剂量组TNF-α表达较模型组明显降低,差异有统计学意义(P<0.01),贝那普利组和抗心力衰竭颗粒中、大剂量组Ⅰ型胶原、Ⅲ型胶原表达较模型组明显降低,差异有统计学意义(P<0.01);Masson染色见贝那普利组及抗心力衰竭颗粒各组胶原沉着较模型组轻。结论抗心力衰竭颗粒能够降低压力超负荷型DHF大鼠心肌TNF-α、Ⅰ型胶原、Ⅲ型胶原的表达,有抑制心肌纤维化的作用。Objective Myocardial fibrosis is an important mechanism of diastolic heart failure (DHF). The aim of the study is to observe the effect of anti-heart-failure granules on TNF-α, collagen of DHF rats, and to discuss the effect of anti-heart-failure granules on myocardial and the treatment mechanism of DHF. Methods Constriction of abdominal aorta was used to build the DHF rats models. The rats were randomized into model group, benazepril group, large, middle, and low doses of anti-heart-failure granules groups, and sham-operation group. Western-blot was used to detect the levels of TNF-ot, collagen I , and collagen IlI. Masson stai- ning was used to observe the deposition of collagen of myocardial cells. Results Compared with the sham operation group, the levels of TNF-α, collagen I and collagen m increased in the model group (P 〈0.01 ). Compared with the model group, the levels of TNF- α decreased in the benazepril group and the anti-heart-failure granules at large dose group ( P 〈 0.01 ). The levels of collagen I and collagen Ill decreased in the benazepril goup and the anti-heart-faiure granules at large and middle groups (P 〈 0.01 ). Masson stai- ning showed a lightened collagen deposition in the benazepril group and the anti-heart-failure granules groups. Conclusion Anti- heart-failure granules can reduce the levels of TNF-α, collagen I , and collagen m in myocardium of DHF rats and then inhibit myo- cardial fibrosis.
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