Objective To establish a rat model of left ventricular hypertrophy ( LVH ) by feeding the rats with high levels of fat,salt,and fructose and to investigate the possible mechanism of action of tea polyphenols ( TP ) in inhibition of LVH.Methods 50 SD rats were divided into normal group and model group.The rats in the model group were fed with high levels of fat,salt,and fructose for 8 weeks.According to blood pressure level ( ＞ 130 mm Hg ),the rats were randomly divided into model control group,captopril group ( 25 mg·kg-1 ),high-dose TP group ( 200 mg·kg-1 ),and low-dose group TP ( 50 mg·kg-1 ) and then were administrated the medications for 4 weeks with the same previous feeding.Blood pressure was examined at an interval of 2 weeks.At the end of medicine administration, the rats was detected by cardiac ultrasound imaging.Serum levels of Ang Ⅱ and TGF-β were determined by enzymelinked immunosorbent assay, and TNF-α level was determined by radioimmunoassay.Obesity index ( OI ),myocardium proliferation index ( MPI ),and cardiac weight index ( CWI ) were measured and calculated.Results As compared with the normal rats,blood pressure was elevated significantly in model rats (P＜0.01);levels of Ang Ⅱ,TNF-α,and TGF-β1 were higher (P＜0.01);OI and MPI were significantly increased (P＜0.05 and P＜0.01）；heart ejection fraction (EF) and left ventricular posterior wall thickness (LVPWT) were increased and left ventricular shortening fraction (FS)was decreased significantly(P＜0.01);E/A value was less than 1 in some model rats.After treatment with TP(200mg·kg-1 or 50mg·kg-1)or captopril,the elevated blood in the model rats markedly declined；and OI and MPI decreased,LVPW and EF were declined significantly (P＜0.01 and P＞0.05),and FS was elevated significantly (P＜0.01 or P＜0.05);no E/A value of ＜1 occurred;levels of Ang Ⅱ,TNF-α,and TGF-β1 were decreased significantly (P＜0.01).Conclusions For this rat model,TP can reduce blood pressure and plays a role in the inhibition of LVH,which may be associated with a decrease in levels of Ang Ⅱ,TNF-α,and TGF-β1.%目的 大鼠给予富含高脂-高盐饲料和果糖饲养,建立左心室肥厚的动物模型,探讨茶多酚( tea polyphenols,TP)抑制左心室肥厚的作用机制.方法 取50只SD大鼠,分为正常组和模型组.模型组大鼠给予富含高脂和高盐的饲料喂养,交替饮用果糖水(6％)和糖盐水(糖4％、盐1％)8周,测定血压.根据血压(＞ 130mm Hg)将动物随机分为模型对照组、卡托普利组( 25 mg·kg-1)、TP高剂量组(200 mg·kg-1)和低剂量组(50 mg·kg-1).继续给予富含高脂-高盐的饲料饲养和交替饮用果糖水和糖盐水,并灌胃给予上述药物处理动物4周.间隔2周测定1次血压,采用小动物超声成像仪检查大鼠心脏功能状态,放射免疫法测定血清TNF-α水平,酶联免疫法测定AngⅡ和TGF-β水平,并测算肥胖指数(OI)、心肌增殖系数(MPI)和心脏系数( CWI).结果 与正常大鼠比较,模型大鼠血压、OI和MPI明显增加(P＜0.05或P＜ 0.01),血清TNF-α、AngⅡ和TGF-β1水平明显升高(P＜0.01)；超声可见大鼠心脏射血分数(EF)增加,左室内膜短轴缩短率(FS)降低,左室后壁厚度( LVPW)增加(P＜0.01),部分大鼠出现E/A值＜1.TP(200 mg·kg-1、50 mg·kg-1)和卡托普利处理后,明显降低模型大鼠血压,降低OI和MPI(P＜0.01),降低EF和LVPW厚度,提高FS(P＜0.05或P＜0.01),未出现E/A值＜1现象；明显降低血清AngⅡ、TNF-α和TGF-β1水平(P＜0.01).结论 TP对高脂-高盐-果糖诱致的左室肥厚模型大鼠,具有降低血压和抑制心室肥厚的作用,可能与降低AngⅡ、TNF-α和TGF-β1水平有关.
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