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目的:探讨茶多酚对高脂-高盐-果糖致左心室肥厚模型大鼠心肌肥厚的防治及其抗氧化作用的影响。方法:取SD大鼠50只,随机分为正常对照组和造模组。除正常对照组大鼠外,其余大鼠均给予高脂-高盐饲料喂养,交替饮用糖盐水(糖4%、盐1%)和果糖水(6%)8 w。根据血压情况,随机将高血压的动物分为模型组(蒸馏水)、卡托普利(25 mg/kg)阳性对照组及茶多酚高(200 mg/kg)、低剂量组(50 mg/kg),每组10只。除正常对照组外,各组动物继续给予高脂-高盐-果糖饲养,同时,分别灌胃给予上述药物处理4 w。测定测算肥胖指数(OI)、心肌增殖系数(MPI)和心脏系数(CWI);取血清分别测定NO和MDA含量及NOS和SOD活性的变化;取左心室心肌组织做病理学检查。结果:与模型组比较,茶多酚处理4 w后,模型大鼠OI和MPI显著,高剂量可降低CWI(P<0.05或P<0.01),对损伤和肥大的心肌具有改善和抑制肥大作用并能显著降低NO和MDA含量及NOS活性,提高SOD活性(P<0.01)。结论:茶多酚对高脂-高盐-果糖诱致左心室肥厚大鼠具有抑制心肌肥大和心肌损伤作用,其机理可能与增强机体抗氧化能力有关。
Objective: To investigate the effect of tea polyphenols on the prevention and treatment of myocardial hypertrophy induced by high fat - high salt - fructose in rats with left ventricular hypertrophy. Methods: Fifty SD rats were randomly divided into normal control group and model group. Except rats in normal control group, the other rats were fed with high-fat and high-salt diet. Sugar and salt water (sugar 4%, salt 1%) and fructose water (6%) were alternately consumed for 8 weeks. Hypertensive animals were randomly divided into model group (distilled water), captopril (25 mg / kg) positive control group and high tea polyphenols (200 mg / kg) and low dose group (50 mg / kg), 10 in each group. Except the normal control group, the animals in each group continued to be fed with high fat - high salt - fructose, and the animals were treated with the above drugs by gavage for 4 weeks respectively. The indexes of OI, MPI and CWI were measured and determined. The content of NO and MDA and the activity of NOS and SOD in serum were measured respectively. The left ventricular tissue was taken for pathological examination. Results: Compared with the model group, after treated with tea polyphenols for 4 w, the OI and MPI of the model rats were significant, and the high dose of CWP reduced the CWI (P <0.05 or P <0.01), and improved and inhibited the hypertrophy of myocardium And can significantly reduce NO and MDA content and NOS activity, increase SOD activity (P <0.01). CONCLUSION: Tea polyphenols can inhibit cardiac hypertrophy and myocardial injury induced by high fat - high salt - fructose in rats with left ventricular hypertrophy, and its mechanism may be related to the enhancement of antioxidant capacity.