摘要
目的研究花色苷矢车菊素-3-葡萄糖苷(C3G)体外抗氧化和改善胰岛素抵抗的活性,并对其中的机制进行探讨。方法利用葡萄糖氧化酶(GO)产生低浓度H_2O_2诱导建立胰岛素抵抗脂肪细胞模型,观察C3G对3T3-L1脂肪细胞内活性氧(ROS)水平和葡萄糖摄取能力的影响;同时检测c-Jun氨基端激酶(JNK)活化和胰岛素信号传导情况。结果 GO处理12h,使细胞ROS水平升高至对照细胞的4.7倍,而胰岛素刺激后对葡萄糖的摄取降低约54%(P<0.01)。C3G能够显著减少GO处理细胞内ROS积聚,抑制JNK活化,增加胰岛素刺激后细胞对葡萄糖的摄取,促进胰岛素受体底物-1酪氨酸磷酸化和葡萄糖转运体-4易位,效应呈浓度依赖型。结论 C3G(≥20μmol/L)可以有效改善氧化应激引起的脂肪细胞胰岛素抵抗。
Objective To explore the bioactivity and mechanism of anthocyanin in protection against oxidative stress-induced insulin resistance in vitro. Methods A typical anthocyanin, cyanidin 3- glucoside （C3G）, was used to evaluate the influence on intracellular ROS level and insulin-stimulated glucose uptake in 3T3-L1 adipocytes that were treated with glucose-oxidase （GO） generated H2O2 for 12h. Results Compared with control adipocytes, treatment with GO led to 4.7-fold increase of intracellular ROS accumulation and 54% reduction of the insulin-stimulated glucose uptake （P〈 0.01）. C3G suppressed the intracellular ROS generation and enhanced insulin-dependent glucose uptake, inhibited the activation of JNK and improved insulin signal transduction in adipocytes in a dose-dependent manner. Conclusions Anthocyanin C3G could protect 3T3-L1 adipocytes against oxidative stress-induced insulin resistance.
出处
《中国糖尿病杂志》
CAS
CSCD
北大核心
2010年第9期650-653,共4页
Chinese Journal of Diabetes
基金
国家自然科学基金项目(30800913)
广东省自然科学基金项目(8451200501000168)
关键词
花色苷
氧化应激
胰岛素抵抗
Anthocyanin
Oxidative stress
Insulin resistance
