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作 者:闫磊[1] 张继东[1] 黄山英[2] 王博[1] 任敏[1] 乔云[1] 吕怡静[1] 郭雪峰[1]
机构地区:[1]山东大学齐鲁医院 中医科 [2]山东大学齐鲁医院教育部和卫生部心血管重构和功能研究重点实验室,济南250012
出 处:《山东大学学报(医学版)》2013年第1期12-16,21,共6页Journal of Shandong University:Health Sciences
基 金:国家自然科学基金(30873324);山东省科技发展计划(2010GWZ20242)
摘 要:目的观察芩丹胶囊(QD)通过激活PPARγ抑制自发性高血压大鼠(SHR)心肌肥厚及心肌组织NF-κB的蛋白表达,探讨QD逆转高血压心室肥厚的作用机制。方法将自发性高血压大鼠(SHR)随机分为模型组(SHR组)、QD大剂量组(SHR+QDH组)、QD小剂量组(SHR+QDL组)、替米沙坦组(SHR+Tel组),WΚY大鼠作为对照组,WKY组同时灌胃给予等量生理盐水。尾袖体表描记法测量各组大鼠收缩压;HE染色观察大鼠心肌组织的改变;透射电镜观察心肌超微结构变化;免疫组化法观察PPARγ和NF-κB蛋白在心肌组织的表达。结果与SHR组相比,SHR+QDH组、SHR+QDL组和SHR+Tel组收缩压均下降(P<0.05);在心肌组织中,PPARγ蛋白表达增高,NF-κB蛋白表达降低(P均<0.05);SHR+QDH组比SHR+QDL组效果更显著(P<0.05)。结论 QD可能通过激活心肌PPARγ,从而阻遏心肌肥厚相关蛋白NF-κB的表达,对改善和逆转高血压心室肥厚起着有益的作用。Objective To observe the effects of Qindan Capsule (QD) on inhibition of ventricular hypertrophy and the expression of NF-KB in spontaneously hypertensive rats (SHR) by way of activating PPARγ so as to investigate the mechanism of QD reversing hypertension ventricular hypertrophy. Methods Spontaneously hypertensive rats (SHR) were divided into the model group( SHR group), QD high dosage group( SHR + QDH group), QD low dosage group ( SHR + QDL group), and SHR + Telmisartan group( SHR + Tel group). Wistar-Kyoto group(WKY) rats of the same weeks were taken as the normal control( WKY group). All rats were administered with corresponding medicine or nor- mal saline. Animal blood pressures were measured by tail-cuff plethysmography. Morphological changes of myocardial tissue were evaluated by HE staining. Ultramicrostructural changes of myocyte were determined by transmission electron microscopy. Expressions of PPAR-γ and NF-KB were detected by immunohistochemical staining. Results Compared with those of the SHR group, the systolic blood pressures and the myocardial expressions of NF-KB in the SHR + QDH group, SHR + QDL group and SHR + Tel group were significantly reduced by QD or Tel ( P 〈 0.05). In the contrast, the myocardial expressions of PPARγ in the SHR + QDH group, SHR + QDL group and SHR + Tel group increased by QD or Tel compared to those of the SHR group ( P 〈 0.05 ). The extent of ventricular hypertrophy in the SHR + QDH group was drasticly less than that in the SHR + QDL group ( P 〈 0.05 ). Conclusion QD ameliorates the ventricular hypertrophy by enhancing the PPARγ expression so as to suppressing the NF-KB expression in myocyte.
关 键 词:芩丹胶囊 心室肥厚 自发性高血压大鼠 过氧化物酶增殖物激活受体Γ 核因子-ΚB
分 类 号:R544.1[医药卫生—心血管疾病] R285.5[医药卫生—内科学]
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