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机构地区:[1]湖北科技学院基础医学院,湖北咸宁437100
出 处:《中国实验方剂学杂志》2014年第11期151-155,共5页Chinese Journal of Experimental Traditional Medical Formulae
基 金:湖北省教育厅科学技术研究项目(B20122804);湖北科技学院科学研究项目(BK1104;ZX1201)
摘 要:目的:探讨粉防己碱对肾性高血压大鼠肥厚左心室肌中心肌营养素-1(CT-1)及其受体复合物gp130/白血病抑制因子受体(LIFR)表达的影响。方法:采用左侧肾动脉部分缩窄法建立大鼠两肾一夹型肾性高血压模型。大鼠随机分为4组(n=15):①假手术组,②高血压模型组,③低剂量粉防己碱组和④高剂量粉防己碱组。③,④组于肾动脉缩窄术后第5周开始分别ig粉防己碱25,50 mg·kg-1·d-1。检测大鼠术后12周末血压(标准尾套法)、左心室重/体重(LVW/BW)、心肌胶原含量、心肌CT-1,gp130和LIFR mRNA以及蛋白表达量。结果:高血压模型组大鼠肥厚心肌中CT-1 mRNA以及蛋白表达增多(P<0.01),而LIFR mRNA以及蛋白表达减少(P<0.01)。应用粉防己碱治疗在抑制高血压大鼠心肌肥厚的同时,也剂量依赖性减少CT-1 mRNA以及蛋白表达量(P<0.01),并提高LIFR mRNA以及蛋白表达量(P<0.01)。结论:粉防己碱可抑制肾性高血压大鼠左室心肌结构性重塑的发生,其作用机制可能与调节心肌组织中心肌营养素-1及其受体gp130/LIFR表达相关。Objective: To investigate the effects of tetradrine on cardiotrophin-1 (CT-1) and its receptor gp130/leukemia inhibitory factor receptor (LIFR) expression in hypertrophic left ventricles of renohypertensive rats. Method: Two-kidney-one-clip (2K1 C) renohypertensive model was established in rats by partial constriction of left renal artery. All the rats were randomly divided into four groups ( n = 15 per group ) : ① sham-operated group; ② hypertensive model group; ③-④ low-dose, high-dose tetradrine group, the hypertensive rats were treated with tetradrine (25, 50 mg·kg^-1·d^-1 ) for 8 weeks. After drug treatment for 8 weeks, the rats were used to measure blood pressure by the standard tail-cuff method, the ratio of left ventricle weight to body weight ( LVW/ BW), myocardial collagen content, and mRNA and protein expressions of CT-1, gpl30 and LIFR. Result: Compared with sham-operated group, the hypertensive model group exhibited a marked increase in the mRNA and protein expression of CT-1 in hypertrophic myocardium (P 〈 0.01 ) , but showed a significant decrease in LIFR mRNA and protein expression (P 〈 0. 01 ). Treatment with tetradrine inhibited the myocardial hypertrophy of hypertensive rats, decreased the expression of CT-1 mRNA and protein (P 〈 0.01 ) , and increased the mRNA and protein expression of LIFR (P 〈 0.01 ). Conclusion: Our findings suggested that treatment with tetradrine could inhibit myocardial structural remodeling in the left ventricles of renohypertensive rats, the mechanism of which might be related to its regulation of the signaling pathway involving cardiotrophin-1 and its receptor gp130/LIFR.
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