【摘要】 目的探讨咖啡酸苯乙酯(CAPE)对2型糖尿病(T2DM)大鼠肝脏的保护作用及其作用机制。方法 24只雄性SD大鼠随机分为3组,即空白组,损伤组,保护组。高脂高糖饲料喂养联合链脲佐菌素诱导建立2型糖尿病大鼠模型,建模成功后,保护组大鼠CAPE灌胃一个月,测量血清中总胆固醇(TC)和甘油三酯(TG)的含量,并对肝脏中丙二醛(MDA)、蛋白羰基化(PCO)的含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性进行测定。结果损伤组血清中总胆固醇(TC)和甘油三酯(TG)明显上升,说明糖尿病大鼠血脂升高。在损伤组中MDA、PCO含量明显升高,而保护组MDA、PCO的含量较损伤组减少(P<0.05),说明糖尿病能够增加肝脏的氧化应激,诱导氧化损伤,而咖啡酸苯乙酯的保护能够降低MDA、PCO的含量,减少氧化损伤;而SOD、CAT在损伤组中含量降低,可能是机体出现的一种自我保护反应,使得机体本身的抗氧化物质大量消耗,咖啡酸苯乙酯可以减少SOD、CAT含量的增加,保护作用比较明显。结论糖尿病的发生可能增加机体的氧化应激,咖啡酸苯乙酯能够有效降低其氧化损伤程度,从而起到对糖尿病肝脏的保护作用。更多还原

【Abstract】 Objective To study the protective effect of caffeic acid phenethyl ester( CAPE) on liver in type 2 diabetic rats( T2DM)and its possible mechanism. Methods 24 male SD rats were randomly divided into three groups,high fat and high sugar diet combined with streptozotocin were used to construct the animal model of type 2 diabetic rat,coffeeic acid phenethyl ester were administrated by month after the models were successfully built,the content of serum triglyeride( TG) and total cholesterol( TC) were measured,meanwhile,the oxidative stress in liver were also assayed,including liver malondialdehyde( MDA),protein carbonyl of( PCO),superoxide dismutase( SOD),catalase( CAT). Results Serum total cholesterol( TC) and triglyeride( TG) in Injury group increased significantly,indicating that the blood lipid in diabetic rats have risen. In injury group,MDA and PCO was significantly increased and the effect of CAPE can reduce the amount of MDA and PCO,indicating diabetes can increase the level of hepatic oxidative stress,finally induced oxidative damage,and CAPE administration can reduce the content of MDA and PCO,relieving the oxidative damage; meanwhile,SOD and CAT were reduced in injury group,It may be related to self-protective response in body,and it’ s obvious that CAPE can relieving the reduce of SOD and CAT contents. Conclusion Diabetes may associate with oxidative stress,CAPE can effectively reduce the degree of oxidative damage,and play a protective effect on diabetic liver.更多还原