CAJ | 학술논문

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.
목적 대서급여부함고지-고염사료화과당사양,건립좌심실비후적동물모형,탐토다다분( tea polyphenols,TP)억제좌심실비후적작용궤제.방법 취50지SD대서,분위정상조화모형조.모형조대서급여부함고지화고염적사료위양,교체음용과당수(6％)화당염수(당4％、염1％)8주,측정혈압.근거혈압(＞ 130mm Hg)장동물수궤분위모형대조조、잡탁보리조( 25 mg·kg-1)、TP고제량조(200 mg·kg-1)화저제량조(50 mg·kg-1).계속급여부함고지-고염적사료사양화교체음용과당수화당염수,병관위급여상술약물처리동물4주.간격2주측정1차혈압,채용소동물초성성상의검사대서심장공능상태,방사면역법측정혈청TNF-α수평,매련면역법측정AngⅡ화TGF-β수평,병측산비반지수(OI)、심기증식계수(MPI)화심장계수( CWI).결과 여정상대서비교,모형대서혈압、OI화MPI명현증가(P＜0.05혹P＜ 0.01),혈청TNF-α、AngⅡ화TGF-β1수평명현승고(P＜0.01)；초성가견대서심장사혈분수(EF)증가,좌실내막단축축단솔(FS)강저,좌실후벽후도( LVPW)증가(P＜0.01),부분대서출현E/A치＜1.TP(200 mg·kg-1、50 mg·kg-1)화잡탁보리처리후,명현강저모형대서혈압,강저OI화MPI(P＜0.01),강저EF화LVPW후도,제고FS(P＜0.05혹P＜0.01),미출현E/A치＜1현상；명현강저혈청AngⅡ、TNF-α화TGF-β1수평(P＜0.01).결론 TP대고지-고염-과당유치적좌실비후모형대서,구유강저혈압화억제심실비후적작용,가능여강저AngⅡ、TNF-α화TGF-β1수평유관.
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.