三黄降糖方对糖尿病大鼠心肌局部肾素-血管紧张素系统的作用

作者	单位
邓常清	广州中医药大学第一附属医院糖尿病研究所
熊曼琪	广州中医药大学第一附属医院糖尿病研究所
邝秀英	广州中医药大学第一附属医院糖尿病研究所
何敏	广州中医药大学第一附属医院糖尿病研究所
李赛美	广州中医药大学第一附属医院糖尿病研究所
朱章志	广州中医药大学第一附属医院糖尿病研究所
徐秋英	广州中医药大学第一附属医院糖尿病研究所
张青云	广州中医药大学第一附属医院糖尿病研究所

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中文摘要:

目的研究三黄降糖方对糖尿病大鼠心肌病变的作用及对心肌肾素 -血管紧张素系统 (RAS)的影响。方法腹腔注射链脲菌素 (STZ)造成大鼠糖尿病模型 ,于造模后 2周起分别灌胃三黄降糖方 (5 0 g/kg)、达美康 (2 0mg/kg)、卡托普利 (15mg/kg)和尼群地平 (30mg/kg) ,连续 8周 ,检测空腹血糖、血清胰岛素(Ins)、心脏 /体重比值及心肌血管紧张素Ⅱ (AngⅡ )、血管紧张素转换酶 (ACE)和醛固酮 (ALD) ,以逆转录-聚合酶链式反应 (RT -PCR)检测心肌血管紧张素 1型受体 (AT1R)mRNA表达。结果与正常对照组比较 ,模型对照组空腹血糖升高 (P <0 0 1) ,血清Ins水平降低 (P <0 .0 1) ,心脏 /体重比值升高 (P <0 .0 1) ,心肌AngⅡ含量增加 (P <0 .0 1) ,ACE活性升高 (P <0 .0 1) ,ALD含量增加 (P <0 .0 5 ) ,心肌AT1RmRNA表达增加 (P <0 .0 5 )。三黄降糖方、达美康、卡托普利和尼群地平均可使模型大鼠血糖轻微降低 ,但各药均不升高血清Ins水平。三黄降糖方、达美康、卡托普利和尼群地平均可使心脏 /体重比值下降 ,心肌AngⅡ含量、ACE活性和AT1RmRNA表达量均下降 ,三黄降糖方和卡托普利还可使心肌ALD含量降低。结论在糖尿病病程 10周 ,可引起心肌肥大 ,心脏局部RAS激活与糖尿病心肌病变的发生有关 ;三黄降糖方、达美康、卡托?

英文摘要:

ObjectiveTo study the effect of Sanhuang Jiangta ng recipe (SJR) on renin-angiotensin system in local myocardium in diabetic rat s. Methods Rats were made into diabetes model by intraperitoneally administering of streptozocin,and medicated through gastrogavage with SJR (50 g/kg),gliclazide (20mg/kg),captopril (15mg/kg) and nitrendipine (30mg/kg) respectively,for successive 8 weeks,started from 2 wee ks after mod eling. Levels of fasting blood sugar (FBS),serum insulin (Ins),heart/body weig ht ratio (H/BW),myocardial angiotensin Ⅱ(Ang Ⅱ),angiotensin converting enzym e (ACE) and aldosterone (ALD) were determined. And the mRNA expression of type Ⅰ angiotensin receptor (AT1R) in myocardium were detected by RT-PCR assay. ResultsAs compared with those in the normal rats,level s of FBS,H/BW,AngⅡ,ACE,ALD and AT1R mRNA expression were higher (all P<0.05) and level of serum Ins was lower (P<0.01) in the model rats. SJR,gliclazide,captopril and nitrendipine could slightly r educe the bloo d sugar level in model rats,but with no increase of serum Ins. All the four dru gs could reduce H/BW,AngⅡ,ACE and AT1R mRNA expression. SJR and captopril cou ld also decrease the ALD content in myocardium.Conclusion Cardiac hypertrophy has been induced in 10 we eks after diabetic modeling. Activation of local myocardial RAS is related to th e genesis of diabetic cardiomyopathy. SJR,gliclazide,captopril and nitrendipin e could antagonize the genesis of diabetic cardiomyopathy,the mechanism is rela ted to the inhibition of RAS activation in local myocardium.

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