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作 者:郑丽丽[1] 王建功[1] 蒋晓钦[1] 张胜利[1] 付向华[2] 张英鸽[3]
机构地区:[1]中国人民解放军460医院心内科,郑州450007 [2]河北医科大学第二附属医院心内科,石家庄050017 [3]军事医学科学院毒物药物研究所,北京100850
出 处:《郑州大学学报(医学版)》2002年第1期45-47,共3页Journal of Zhengzhou University(Medical Sciences)
摘 要:目的:研究血管紧张素Ⅱ(AngⅡ)AT1受体拮抗剂氯沙坦对大鼠血管成形术后血管平滑肌细胞(VSMCs)转化生长因子β受体(TβR)和纤连蛋白(FN)表达的影响。方法:Wistar雄性大鼠24只,随机分为3组,对照组、血管损伤组、氯沙坦组,每组8只。血管损伤组和氯沙坦组均行血管成形术,氯沙坦组于手术前7d起给予氯沙坦20mg·kg-1·d-1灌胃,余 2组以等量生理盐水灌胃。术后 14 d处死全部动物,取胸主动脉 2 cm,用 RT-PCR及 North-ern杂交方法测定 VSMCs TβRⅠ、TβRⅡ及 FN mHNA的表达。结果:血管损伤组TβRⅠ、TβR Ⅱ、FN mRNA的表达较对照组明显增高(P<0.001),氯沙坦则对其表达有明显抑制作用(P<0.01)。结论:氯沙坦通过抑制VSMCs TβRⅠ、TβR Ⅱ表达,从而抑制细胞外基质(EMC)的形成可能是其防治再狭窄的作用机制之一。Aim: To investigate the effects of losartan, an angiotensin Ⅱ AT1 receptor antagonist, on the mRNA expressions of transforming growth factor β receptors(TβR Ⅰ and TβRⅡ ) and fibronectin (FN) in the vascular smooth muscle cells (VSMCs) of the thoracic aorta after angioplasty in the rats. Methods: A total of 24 Wistar male rats were randomly divided into the vascular injury, losartan treatment, and control groups. Each group had 8 rats. The vascular injury and losartan groups were both performed angioplasty . Losartan was affused into the rats' stomach with the dosage of 20 mg· kg-1· d-1 beginning from the 7th d before the operation for the losartan treatment group. The equivalent volume of physiological saline was affused into the rats' stomach for the vascular injury and control groups. All the animals were executed on the 14th d after the operation. Two centimeter thoracic aorta was taken to examine the mRNA expressions of TβR Ⅰ , TβRⅡ , and FN in VSMCs by RT-PCR and Northern blot methods. Results: The mRNA expressions of TβRⅠ , TβRⅡ and FN in VSMCs were significantly higher in vascular injury group than those in control group( P < 0.001) .Losartan had obviously suppressing effect on these expressions. Conclusions: Our study indicates that one of the mechanisms for preventing restenosis of losartan after angioplasty is to reduce the formation of extracelluar matrix by suppressing the mRNA expressions of TβRⅡ ,TβRⅡ , and FN in the VSMCs in the rats.
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