咖啡酸苯乙酯对肥胖小鼠氧化应激状态调节作用研究

目的]明确肥胖发生机制,并考察咖啡酸苯乙酯(CAPE)对肥胖小鼠体内氧化应激状态的调节作用。方法]采用营养饲料(含有高组分的糖、蛋白以及脂肪)喂养昆明系小鼠4周,建模成功后随机分组,CAPE注射组分别给予不同剂量的CAPE,继续喂养50 d,测定其体重、脂体比和肝脏比重;测量其血清中总胆固醇(TC)和甘油三酯(TG)含量,并对其肝脏氧化损伤指标:脂质过氧化反应(LPO)、蛋白羰基化(PCO)以及体内抗氧化防御系统:谷胱甘肽(GSH)和过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的活性进行了测定。结果]营养饲料能够促进小鼠体重(P0.01)、体脂含量(P0.05)以及肝脏比重(P0.05)的增加,提高其血清中TC、TG水平,有利于小鼠肥胖的发生;CAPE能够缓解小鼠体重、脂体比以及肝脏比重的增加(P0.05),同时肥胖会影响小鼠体内氧化应激状态,导致其氧化损伤程度增加,且抗氧化酶活性发生变化;CAPE能够缓解体内氧化应激状态,调节体内抗氧化酶的活性。结论]氧化应激可能参与肥胖的发生,CAPE有望通过其抗氧化作用调节体内的氧化压力起到抑制肥胖发生的作用。

Study on the Effect of Caffeic Acid Phenethyl Ester (CAPE) on the Oxidative Stress in Obesity Mice

Objective] The aim was to define the obesity mechanism,and investigate the regulating effect of CAPE on the oxidative stress in obesity mice.Methods] Kunming mice were fed by nutrition feeds(contain high component sugar,protein and fat) for 4 weeks,after successful modeling,the mice were randomly assigned and injected different dosages of CAPE for 50 d,at the end of experiment,the weight of mice and the ratio of fat weight /weight,liver weight/weight were also counted,the content of serum triglyeride(TG) and total cholesterol(TC) were measured,meanwhile,the oxidative stress in liver were also assayed,including the oxidative damage parameters(lipid perioxidation(LPO),protein carbonxyl(PCO)) and the antioxidative system(catalase(CAT),superoxidase(SOD),reduced glutamine(GSH)).Result] It was revealed that the feeding of nutrition can prompt the formation of obesity mice,and oxidative stress may be involved in the occurrence of obesity,however,the effect of CAPE can relieve the occurrence of obesity and reduce the weight of mice(P<0.05),the ratio of fat weight/mice weight(P<0.05) and the ratio of liver weight/mice weight(P<0.05),in addition,CAPE can attenuate the oxidative stress in obesity mice by reducing the content of LPO and PCO and altering the activities of CAT,SOD and GSH.Conclusion] The antioxidative effect of CAPE may involve in the effect of reducing the occurrence of obesity and relieving the oxidative stress induced by obesity.