摘要
目的探讨高糖状态下晚期糖基化终产物(AGEs)诱导大鼠肾小管上皮细胞株NRK-52E氧化应激及普罗布考干预作用。方法作用72 h后,用Western Blot检测空白对照组(0 mmol/L葡萄糖)、高糖组(25 mmol/L葡萄糖)、AGEs组(100mg/L AGEs)、高糖AGEs组(100 mg/L AGEs加25 mmol/L葡萄糖)、普罗布考预处理高糖AGEs组(100μmol/L普罗布考加100 mg/L AGEs加25 mmol/L葡萄糖)中核因子κB(NF-κB)及肿瘤坏死因子-α(TNF-α)在NRK-52E细胞的表达。用CM2H2DCFDA试剂检测活性氧(ROS)含量。结果高浓度葡萄糖及AGEs均上调NF-κB及TNF-α表达。普罗布考显著抑制调高浓度葡萄糖状态下AGEs诱导NF-κB及TNF-α表达,以及抑制ROS生成。结论普罗布考能抑制高浓度葡萄糖状态下AGEs诱导细胞氧化应激。
Objective To study whether probucol had affected advanced glycation end-products（AGEs） under high glucose inducing oxidative stress in NRK-52E.Methods NF-κB and TNF-α were detected Western Blot in control group（0 mmol/L glucose）,high glucose group（25 mmol/L glucose）,AGEs goup（100mg/L AGEs）,AGEs and high glucose group（100mg/L AGEs＋25mmol/L glucose）,probucol group（100 μmol/L probucol＋100 mg/L AGEs＋25 mmol/L glucose） had carried out after 72 h.Then ROS were detected by CM2H2DCFDA.Results The expression of NF-κB and TNF-α were up-regulated by high glucose and AGEs,probucol could also down-regulate NF-κB and TNF-α induced by AGEs under high glucose condition.probucol also could decrease ROS which were increased by high glucose and AGEs.Conclusion AGEs under high glucose condition can induce oxidative stress,but which can be inhibited by probucol in NRK-52E.
出处
《重庆医学》
CAS
CSCD
北大核心
2010年第20期2737-2738,共2页
Chongqing medicine
