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作 者:马丽[1,2] 蒋梅先[2] 张超[2] 姚成增[2] 周洪武[2] 阮晓芬[2]
机构地区:[1]新疆医科大学附属中医医院,乌鲁木齐830000 [2]上海中医药大学附属曙光医院,上海200021
出 处:《中华中医药杂志》2012年第9期2454-2457,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:上海市科委课题(No.034119846)~~
摘 要:目的:探讨坎离颗粒对腹主动脉缩窄所致心衰大鼠心肌间质重构的影响及可能作用机制。方法:腹主动脉缩窄法制备大鼠心衰模型,分为模型组、中药组(坎离颗粒)和阳性对照组(卡托普利),另设假手术组,每组15只;造模12周后各治疗组分别给予坎离颗粒水溶液12g.kg-1.d-1和卡托普利混悬液3.375mg.kg-1.d-1,假手术组和模型组给予等量双蒸水。干预24周后处死大鼠,检测左室质量指数(LVMI)、左室腔内径(LVD)、左室后壁厚度(LVPWT);苦味酸天狼猩红染色测量胶原容积分数(CVF);免疫组化法测量心肌左室心肌基质金属蛋白酶-9(MMP-9)、基质金属蛋白酶抑制剂-1(TIMP-1)、转化生长因子-β1(TGF-β1)的含量。结果:坎离颗粒可降低CVF、心脏指数(P<0.05)和LVMI(P<0.01),升高I/Ⅲ型胶原比值(P<0.05)、LVD(P<0.01);纠正心衰大鼠心肌的TGF-β1(P<0.01)、MMP-9(P<0.01)、TIMP-1(P<0.05)异常表达,部分指标优于对照组。结论:坎离颗粒可能通过减少心肌MMP-9、TGF-β1和增加TIMP-1的含量,而减轻心肌胶原网络的破坏及反应性胶原的过度沉积,从而改善心肌间质重构,改善心脏功能。Objective: To investigate the effect and its mechanism of Kanli Granule on myocardial extracellular matrix remodeling in chronic heart failure by partial coarctation of abdominal aorta in rats. Methods: The chronic heart failure model was induced by partial coarctation of abdominal aorta in rats, 45 CHF model rats induced by constriction were divided into 3 groups, the aortic stenosis (BD), Kanli+BD and Captopril+BD, meanwhile, sham-operated rats were established as the control group. 24 weeks after operation, the mass index (CMI) and left ventricular mass indices (LVMI), including LVd, LVPW were measured pathologically. Myocardial cell and interstitial collagen were observed by HE and VG stain. The expression of MMP-9, TIMP-1, TGF-[31 was detected by immune-histochemical method. Results: the animal study showed that Kanli Granule markedly decreased collagen volume fraction, cardiac mass index (P〈0.05) and left ventricular mass indices (P〈0.01) including LVMI, LVD, meanwhile increased ratio of type I/II (P〈0.05) but it increased LVPW; it also rectified abnormal expression of TGF-β1, MMP-9 and TIMP-I in failing rat myocardium with some better results favoring captopril group (P〈0.01, P〈0.05). Conclusion: Kanli Granule can keep down the concentration of MMP-9, TGF-β1 in myocardium of rats with CHF elevate the TIMP-1, control over- degradation of myocardial collagen and prevent ventricle expanding which was related to relieving the myocardial extracellular matrix remodeling of CHF.
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