松龄血脉康胶囊对自发性高血压大鼠PPARγ调控机制的实验研究

目的研究松龄血脉康胶囊对自发性高血压大鼠（SHR）血压的影响以及对过氧化物酶体增殖物激活受体γ（peroxisome proliferator activated receptor-γ， PPARγ）的调节机制。方法 24只10周龄SHR大鼠随机分为空白组、中药组和西药组，每组8只。中药组灌胃松龄血脉康20 mg/（kg?d）；西药组灌胃雷米普利1 mg/（kg?d）；空白组给予同体积的生理盐水。每周测血压1次，4周后检测心脏超声；腹主动脉取血处死动物，荧光实时定量PCR技术检测肝脏PPARγ 和血管紧张素Ⅱ 1型受体（AT1R）mRNA的表达水平。免疫组织化学（SP法）染色观察PPARγ和AT1R蛋白的表达，蛋白印迹定量分析PPARγ和AT1R的含量。结果用药4周后，中药组血压降低，与空白组比较，差异有统计学意义（P<0.01）。中药降压效果不如西药明显，但整体来看，中药较西药降压稳定，能够使血压维持在相对稳定的水平；中药组心脏射血分数增高，并显著上调肝脏PPARγ mRNA表达及肝脏PPARγ蛋白水平，与空白组比较，差异均有统计学意义（P<0.05，P<0.01）；中药组AT1R mRNA表达明显抑制，AT1R蛋白水平下调，与空白组、西药组比较，差异均有统计学意义（P<0.01）。结论松龄血脉康胶囊通过上调PPARγ mRNA的表达和蛋白合成，抑制AT1R mRNA的表达和蛋白合成，可能是其抑制血压升高，提高心脏射血分数的部分作用机制。

英文摘要:

Objective To study the effect of Songling Xuemaikang Capsule （SXC） on blood pressure of spontaneously hypertensive rats （SHR） and regulatory mechanisms for peroxisome proliferator activated receptor-γ （PPARγ）. Methods Totally 24 10-week-old SHR rats were randomly divided into the blank control group， the Chinese medicine （CM） group， and the Western medicine （WM） group， 8 in each group. Rats in the CM group were administered with SXC at the daily dose of 20 mg/kg by gastrogavage. Those in the WM group were administered with ramipril at the daily dose of 1 mg/kg by gastrogavage. Those in the blank control group were administered with equal volume of normal saline. The blood pressure was measured once per week. The cardiac ultrasound was performed 4 weeks later. Rats were killed and then blood was sampled from abdominal aorta. mRNA expressions of liver PPARγ and angiotensin 〖STBZ〗Ⅱ 〖WT9.75《Helvetica》〗 type 1 receptor （AT1R） were detected by fluorescence real-time quantitative PCR. Protein expressions of PPARγ and AT1R were detected using immunohistochemical assay （SP）. The contents of PPARγ and AT1R were quantitatively analyzed by Western blot. Results After 4 weeks of treatment， the blood pressure decreased in the CM group， showing statistical difference when compared with the blank control group （P<0.01）. CM was inferior to WM in lowering blood pressure. But as a whole， CM was more stable and could maintain blood pressure at a relatively stable level. The cardiac ejection fraction increased in the CM group， showing statistical difference when compared with the blank control group （P<0.05， P<0.01）. The mRNA and protein expressions of liver PPARγ were up-regulated in the CM group， showing statistical difference when compared with the blank control group （P<0.05，P<0.01）. CM could obviously inhibit the AT1R mRNA expression， and down-regulate the protein expression of AT1R， showing statistical difference when compared with the blank control group and the WM group respectively （P<0.01）. Conclusion SXC decreased blood pressure and improved the cardiac ejection fraction， which might be partially achieved by up-regulating the PPARγ mRNA expression and protein synthesis， and inhibiting the AT1R mRNA expression and AT1R protein synthesis.

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