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目的 :比较茶多酚 (TP)、槲皮素 (Que)和维生素C(Vc)的体内外抗氧化作用 ,并分析其构效关系。方法 :采用 4个体外氧化应激模型 :在大鼠的心、脑匀浆和CCl4毒化小鼠肝脏匀浆中用Fenton反应诱导脂质过氧化模型 ,以及H2 O2诱导红细胞溶血模型 ;3个体内模型 :结扎小鼠大脑中动脉 (MCAO)致脑梗塞模型 ,大鼠冠脉缺血再灌注致心律失常模型和CCl4毒化致小鼠肝损伤模型。分别测定了各化合物在这些模型中的抗氧化作用。结果 :在体外 ,Que和TP均可剂量依赖性地抑制Fenton反应导致的大鼠心、脑匀浆和CCl4毒化小鼠肝匀浆中过氧化脂质 (LPO)的生成和H2 O2 诱导的红细胞溶血 :Que的IC50 分别为 :0 4× 10 -4,0 2× 10 -4,0 5× 10 -4,0 3× 10 -4mol/L ;TP的IC50 分别为 :0 7× 10 -4,7 8× 10 -4,1 1×10 -4,0 6× 10 -4mol/L。二者的作用均大大优于Vc(IC50 分别为 110× 10 -4,<0 0 0 1,2 1× 10 -4,2 9× 10 -4mol/L)。在体内 ,2 0mg/kg剂量的Que和TP以及 2 0 0mg/kg剂量的Vc均可有效改善MCAO小鼠的运动功能障碍 ,缩小脑梗塞面积 (ip抑制率分别为 32 % ,2 4 % ,19% ,po抑制率分别为 2 5 % ,2 0 % ,16 % ) ,减少脑组织中LPO的生成及提高GSH PX的活性 ;还可缩小心律失常大鼠的心肌梗塞范围 (抑制率分别为 2 4
Objective: To compare the antioxidant effects of tea polyphenols (TP), quercetin (Que) and vitamin C (Vc) in vivo and in vitro, and analyze their structure-activity relationship. METHODS: Four in vitro oxidative stress models were used: lipid peroxidation model induced by Fenton reaction in rat heart and brain homogenate and liver homogenate of CCl4-poisoned mice, and H2O2-induced red blood cell hemolysis model; Models: Ligation of middle cerebral artery (MCAO)-induced cerebral infarction model, rat coronary artery ischemia-reperfusion induced arrhythmia model, and CCl4 poisoning-induced liver injury model in mice. The antioxidant effects of each compound in these models were determined separately. RESULTS: In vitro, both Que and TP inhibited the production of lipid peroxides (LPO) and H2O2-induced red blood cells in rat heart and brain homogenate and CCl4-poisoned mouse liver homogenate in a dose-dependent manner. Hemolysis: IC50 of Que were: 0 4 × 10 -4, 0 2 × 10 -4, 0 5 × 10 -4, 0 3 × 10 -4 mol/L; IC50 of TP were: 0 7 × 10 -4 , 7 8×10 -4,1 1×10 -4,0 6×10 -4 mol/L. Both have much better effects than Vc (IC50 110 × 10 -4, <0 0 0 1, 2 1 × 10 -4, and 2 9 × 10 -4 mol/L, respectively). In vivo, 20mg/kg dose of Que and TP and 200mg/kg dose of Vc were effective in improving motor dysfunction and reducing cerebral infarct size in MCAO mice (ip inhibition rates were 32% and 24%, respectively). In 19%, the inhibition rates of po were 25%, 20%, and 16%, respectively, which reduced the production of LPO in the brain and increased the activity of GSH PX; it also reduced the myocardial infarction range in arrhythmic rats (the inhibition rates were twenty four