| 引用本文:曾紫凡1，张惠敏1，任莹璐1，焦世红2，王伟1.基于氧化应激调控的芪参颗粒干预心力衰竭大鼠的机制研究[J].世界中医药,2018,(05):. |
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| 基于氧化应激调控的芪参颗粒干预心力衰竭大鼠的机制研究 |
| Mechanisms of Qishen Granules on Heart Failure Rats by Regulating Oxidative Stress |
| 投稿时间：2017-12-19 |
| DOI：10.3969/j.issn.1673-7202.2018.05.045 |
| 中文关键词: 氧化应激 芪参颗粒 心力衰竭 大鼠 调控 机制 |
| English Keywords:Oxidative stress Qishen granules Heart failure Mechanism |
| 基金项目:国家自然科学基金项目(81530100;81470191);北京中医药大学基本科研业务费自主选题项目(2017-JYB-XS-003;2017-JYB-XS-017) |
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| 中文摘要: |
| 目的:探讨芪参颗粒干预心力衰竭大鼠的药效研究,并基于氧化应激探讨其作用机制。方法:制备左冠脉结扎诱导的心力衰竭大鼠模型,随机分为假手术组、模型组、芪参颗粒组、福辛普利组。通过苏木精-伊红染色(HE)法、Masson染色分别观察各组大鼠心肌病理变化,并采用实时荧光定量PCR(RT-PCR)和蛋白印迹(Western blotting)法分别检测大鼠心肌中氧化应激关键分子p47phox、RAC1的含量。结果:HE染色和Masson染色显示模型组大鼠心肌细胞排列紊乱,丧失正常结构,心肌间质出现大量炎细胞浸润,胶原过度沉积,纤维明显增生;而芪参颗粒与假手术组排列整齐,细胞形态基本无变化,几乎没有沉积的胶原蛋白。RT-PCR和Western blotting显示模型组p47phox、RAC1在mRNA与蛋白层面显著增高;而芪参颗粒可显著降低p47phox、RAC1的含量。结论:芪参颗粒能显著改善左冠脉结扎诱导诱导的大鼠心力衰竭,其机制可能与抑制p47phox、RAC1诱导的氧化应激效应有关。 |
| English Summary: |
| To study the effect and mechanisms of Qishen granules (QSG) on heart failure rats based on oxidative stress. Methods:Heart failure rat model was established by ligation of left coronary artery (LAD). Rats were randomly divided into four groups including sham group, model group, QSG group and Fosinopril group. The pathological changes of heart were assessed by Hematoxylin-Eosin (HE) and Masson's staining. Real-Time PCR and Western blot were respectively used to detect the mRNA and protein levels of p47phox and RAC1, the key molecules in oxidative stress in each group. Results:HE and Masson's staining showed that the myocardial cells of rats in model group were disorderly arranged, and a large number of inflammatory cells were infiltrated in the interstitium. The collagen was excessively accumulated and the fibrous tissue was proliferated. On the contrast, the myocardial cells of rats in QSG and sham group were arranged in an order way and the collagen deposition was hardly observed. Real-Time PCR (RT-PCR) and Western blotting results showed that mRNA and protein levels of p47phox and RAC1 were increased in the model group, and QSG could significantly inhibit the expression of them. Conclusion:QSG may improve the heart function of heart failure rats induced by left anterior descending artery ligation, and its mechanisms is probably related to the inhibition of oxidative stress. |
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