海峡药学
海峽藥學
해협약학
STRAIT PHARMACEUTICAL JOURNAL
2015年
4期
24-26
,共3页
杨含艳%展平%任丽伟%于志文
楊含豔%展平%任麗偉%于誌文
양함염%전평%임려위%우지문
姜黄素%PQ%Nrf2%抗氧化作用%胰岛素抵抗
薑黃素%PQ%Nrf2%抗氧化作用%胰島素牴抗
강황소%PQ%Nrf2%항양화작용%이도소저항
Curcumin%PQ%Nrf2%Anti-oxidative function%Insulin resistance
目的：观察姜黄素是否具有改善百草枯（ Paraquat，PQ）所致氧化应激诱导的胰岛素抵抗作用并探讨其改善胰岛素抵抗的效应机理。方法将实验小鼠随机分成对照组（ Control组），百草枯组（ PQ组）以及PQ加姜黄素组（ Cur组）。 PQ和Cur组连续腹腔注射百草枯7天造模成功后。 Cur组继续Cur灌胃干预。7天后，取胰岛素敏感组织肌肉，用蛋白免疫印迹方法（ Western blot，WB）检测蛋白水平和磷酸化变化，并检测脂质过氧化指标MDA。结果在PQ诱导的小鼠胰岛素抵抗模型中，姜黄素可改善小鼠葡萄糖耐量并对抗 PQ 所致的胰岛素信号蛋白 PKB－Ser473磷酸化损害；姜黄素还可明显降低肌肉MDA水平，激活小鼠Nrf2系统，促进Nrf2核转位和NQO－1的表达，同时能增强IкBα的水平，缓解氧化应激及炎症反应。结论姜黄素通过增强内源性Nrf2系统功能和胰岛素信号水平，对抗PQ诱导的氧化应激，是其缓解胰岛素抵抗的重要机理。
目的：觀察薑黃素是否具有改善百草枯（ Paraquat，PQ）所緻氧化應激誘導的胰島素牴抗作用併探討其改善胰島素牴抗的效應機理。方法將實驗小鼠隨機分成對照組（ Control組），百草枯組（ PQ組）以及PQ加薑黃素組（ Cur組）。 PQ和Cur組連續腹腔註射百草枯7天造模成功後。 Cur組繼續Cur灌胃榦預。7天後，取胰島素敏感組織肌肉，用蛋白免疫印跡方法（ Western blot，WB）檢測蛋白水平和燐痠化變化，併檢測脂質過氧化指標MDA。結果在PQ誘導的小鼠胰島素牴抗模型中，薑黃素可改善小鼠葡萄糖耐量併對抗 PQ 所緻的胰島素信號蛋白 PKB－Ser473燐痠化損害；薑黃素還可明顯降低肌肉MDA水平，激活小鼠Nrf2繫統，促進Nrf2覈轉位和NQO－1的錶達，同時能增彊IкBα的水平，緩解氧化應激及炎癥反應。結論薑黃素通過增彊內源性Nrf2繫統功能和胰島素信號水平，對抗PQ誘導的氧化應激，是其緩解胰島素牴抗的重要機理。
목적：관찰강황소시부구유개선백초고（ Paraquat，PQ）소치양화응격유도적이도소저항작용병탐토기개선이도소저항적효응궤리。방법장실험소서수궤분성대조조（ Control조），백초고조（ PQ조）이급PQ가강황소조（ Cur조）。 PQ화Cur조련속복강주사백초고7천조모성공후。 Cur조계속Cur관위간예。7천후，취이도소민감조직기육，용단백면역인적방법（ Western blot，WB）검측단백수평화린산화변화，병검측지질과양화지표MDA。결과재PQ유도적소서이도소저항모형중，강황소가개선소서포도당내량병대항 PQ 소치적이도소신호단백 PKB－Ser473린산화손해；강황소환가명현강저기육MDA수평，격활소서Nrf2계통，촉진Nrf2핵전위화NQO－1적표체，동시능증강IкBα적수평，완해양화응격급염증반응。결론강황소통과증강내원성Nrf2계통공능화이도소신호수평，대항PQ유도적양화응격，시기완해이도소저항적중요궤리。
OBJECTIVE To observe the effect and explore the mechanism of curcumin on the paraquat-media-ted oxidative stress and insulin resistance.METHODS Thirty mice were randomly divided into 3 groups:control group,paraquat group and curcumin intervention group.Paraquat group and curcumin intervention group were contin-uously intraperitoneal injection of paraquat for 7 days to induce the models of insulin resistance.The curcumin inter-vention group was continuously gavaged with curcumin for another 7 days.Then,all mice were euthanized for muscle collection.The protein and phosphorylation levels in muscle tissue were examed by Western blot and the content of malonaldchyde ( MDA) indicated for lipid peroxidation was determined.RESULTS Curcumin improved the glucose tolerance in paraquat-induced insulin resistance in mice together with attenuation of PQ-caused impairment in PKB-Ser473 phosphorylation.Curcumin also significantly reduced muscular MDA level,promoted the Nrf2 translocation in-to nucleus, enhanced expression of quinine oxidoreductase1 ( NQO-1 ) .Curcumin also increased IкBαcontent.CONCLUSION Curcumin enhances the function of endogenous Nrf2 system and insulin signaling to against PQ-induced oxidative stress and inflammation which may be the mechanisms of curcumin to attenuate insulin resistance.
