中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2015年
3期
226-230
,共5页
二十二碳六烯酸类%棕榈酸%胰岛素抵抗
二十二碳六烯痠類%棕櫚痠%胰島素牴抗
이십이탄륙희산류%종려산%이도소저항
Docosahexaenoic acids%Palmitate acid%Insulin resistance
目的 观察二十二碳六烯酸(DHA)对棕榈酸诱导的C2C12细胞胰岛素抵抗的影响.方法 将C2C12细胞诱导分化成熟,加棕榈酸及DHA处理,通过实时聚合酶链反应(real-Time qPCR)及免疫印迹检测C2C12细胞葡萄糖转运体4(GLUT4)、胰岛素受体-β(IR-β)、胰岛素受体底物-1(IRS-1)、单核细胞趋化蛋白-1(MCP-1)、白细胞介素-6(IL-6)、诱导型一氧化氮合酶(iNOS)表达;谷胱甘肽检测试剂盒检测超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性,荧光分光光度计检测活性氧(ROS);[3H]-2-脱氧-D-葡萄糖检测C2C12细胞葡萄糖摄取量.结果 棕榈酸组与对照组比较,磷酸化胰岛素受体底物-1(P-IRS-1)的表达上调[(2.9±0.3)比(1.1±0.1),P＜0.05];磷酸化胰岛素受体-β(p-IRβ)表达下调[(0.87 ±0.09)比(1.58±0.21),P＜0.05];GLUT4表达下调[(1.1±0.3)比(3.3±0.4),P＜0.05];炎症分子MCP-1、IL-6、iNOS表达明显上升:[MCP-1:(27.2±0.6)比(1.0±0.1),P＜0.001;IL-6:(94.9 ±6.5)比(0.8±0.0),P＜0.001;iNOS:(288.0±15.6)比(1.8±0.6),P＜0.001].C2C12细胞氧化应激标志物ROS升高2.1倍(P＜0.05),SOD、GSH-Px活性分别下降63％及49％(P＜0.05);DHA组与棕榈酸组比较,p-IRS-1的表达下调[(1.3±0.2)比(2.9±0.3),P＜0.05],p-IRβ表达上调[(1.3±0.2)比(0.9±0.1),P＜0.05],GLUT4表达明显升高[(2.8±0.4)比(1.1±0.3),P ＜0.05];炎症分子MCP-1、IL-6、iNOS表达均明显下调[MCP-1:(18.5±0.3)比(27.2 ±0.6),P＜0.001;IL-6:(1.7±0.4)比(94.9±6.5),P＜0.001;iNOS:(5.0±0.9)比(288.0 ±15.6),P＜0.001],氧化应激标志物ROS下降55％(P＜0.05),SOD、GSH-Px活性升高72％及64％ (P ＜0.05).结论 DHA通过激活C2C12细胞的胰岛素信号通路,减少细胞的炎症反应及氧化应激而改善胰岛素抵抗.
目的 觀察二十二碳六烯痠(DHA)對棕櫚痠誘導的C2C12細胞胰島素牴抗的影響.方法 將C2C12細胞誘導分化成熟,加棕櫚痠及DHA處理,通過實時聚閤酶鏈反應(real-Time qPCR)及免疫印跡檢測C2C12細胞葡萄糖轉運體4(GLUT4)、胰島素受體-β(IR-β)、胰島素受體底物-1(IRS-1)、單覈細胞趨化蛋白-1(MCP-1)、白細胞介素-6(IL-6)、誘導型一氧化氮閤酶(iNOS)錶達;穀胱甘肽檢測試劑盒檢測超氧化物岐化酶(SOD)、穀胱甘肽過氧化物酶(GSH-Px)活性,熒光分光光度計檢測活性氧(ROS);[3H]-2-脫氧-D-葡萄糖檢測C2C12細胞葡萄糖攝取量.結果 棕櫚痠組與對照組比較,燐痠化胰島素受體底物-1(P-IRS-1)的錶達上調[(2.9±0.3)比(1.1±0.1),P＜0.05];燐痠化胰島素受體-β(p-IRβ)錶達下調[(0.87 ±0.09)比(1.58±0.21),P＜0.05];GLUT4錶達下調[(1.1±0.3)比(3.3±0.4),P＜0.05];炎癥分子MCP-1、IL-6、iNOS錶達明顯上升:[MCP-1:(27.2±0.6)比(1.0±0.1),P＜0.001;IL-6:(94.9 ±6.5)比(0.8±0.0),P＜0.001;iNOS:(288.0±15.6)比(1.8±0.6),P＜0.001].C2C12細胞氧化應激標誌物ROS升高2.1倍(P＜0.05),SOD、GSH-Px活性分彆下降63％及49％(P＜0.05);DHA組與棕櫚痠組比較,p-IRS-1的錶達下調[(1.3±0.2)比(2.9±0.3),P＜0.05],p-IRβ錶達上調[(1.3±0.2)比(0.9±0.1),P＜0.05],GLUT4錶達明顯升高[(2.8±0.4)比(1.1±0.3),P ＜0.05];炎癥分子MCP-1、IL-6、iNOS錶達均明顯下調[MCP-1:(18.5±0.3)比(27.2 ±0.6),P＜0.001;IL-6:(1.7±0.4)比(94.9±6.5),P＜0.001;iNOS:(5.0±0.9)比(288.0 ±15.6),P＜0.001],氧化應激標誌物ROS下降55％(P＜0.05),SOD、GSH-Px活性升高72％及64％ (P ＜0.05).結論 DHA通過激活C2C12細胞的胰島素信號通路,減少細胞的炎癥反應及氧化應激而改善胰島素牴抗.
목적 관찰이십이탄륙희산(DHA)대종려산유도적C2C12세포이도소저항적영향.방법 장C2C12세포유도분화성숙,가종려산급DHA처리,통과실시취합매련반응(real-Time qPCR)급면역인적검측C2C12세포포도당전운체4(GLUT4)、이도소수체-β(IR-β)、이도소수체저물-1(IRS-1)、단핵세포추화단백-1(MCP-1)、백세포개소-6(IL-6)、유도형일양화담합매(iNOS)표체;곡광감태검측시제합검측초양화물기화매(SOD)、곡광감태과양화물매(GSH-Px)활성,형광분광광도계검측활성양(ROS);[3H]-2-탈양-D-포도당검측C2C12세포포도당섭취량.결과 종려산조여대조조비교,린산화이도소수체저물-1(P-IRS-1)적표체상조[(2.9±0.3)비(1.1±0.1),P＜0.05];린산화이도소수체-β(p-IRβ)표체하조[(0.87 ±0.09)비(1.58±0.21),P＜0.05];GLUT4표체하조[(1.1±0.3)비(3.3±0.4),P＜0.05];염증분자MCP-1、IL-6、iNOS표체명현상승:[MCP-1:(27.2±0.6)비(1.0±0.1),P＜0.001;IL-6:(94.9 ±6.5)비(0.8±0.0),P＜0.001;iNOS:(288.0±15.6)비(1.8±0.6),P＜0.001].C2C12세포양화응격표지물ROS승고2.1배(P＜0.05),SOD、GSH-Px활성분별하강63％급49％(P＜0.05);DHA조여종려산조비교,p-IRS-1적표체하조[(1.3±0.2)비(2.9±0.3),P＜0.05],p-IRβ표체상조[(1.3±0.2)비(0.9±0.1),P＜0.05],GLUT4표체명현승고[(2.8±0.4)비(1.1±0.3),P ＜0.05];염증분자MCP-1、IL-6、iNOS표체균명현하조[MCP-1:(18.5±0.3)비(27.2 ±0.6),P＜0.001;IL-6:(1.7±0.4)비(94.9±6.5),P＜0.001;iNOS:(5.0±0.9)비(288.0 ±15.6),P＜0.001],양화응격표지물ROS하강55％(P＜0.05),SOD、GSH-Px활성승고72％급64％ (P ＜0.05).결론 DHA통과격활C2C12세포적이도소신호통로,감소세포적염증반응급양화응격이개선이도소저항.
Objective To explore the effects of docosahexaenoic acid (DHA) on palmitate-induced insulin resistance in C2C12 cells.Methods Differentiated C2C12 myotubes were used.The gene expression of inflammatory cytokine and insulin signaling pathway were evaluated by quantitative polymerase chain reaction (qPCR) and Western blot.And glucose uptake was measured by [3H]-2DG uptake.The levels of reactive oxygen species (ROS) were evaluated by DCF fluorescence.And the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured with a glutathione assay kit.Results Palmitate-induced cellular insulin resistance was clarified by reduced [3H]-2DG uptake and impaired gene expression of insulin signaling pathway (GLUT4,p-IR3 and p-IRS-1).DHA decreased the expression of palmitate-caused pro-inflammatory cytokines (MCP-1,IL-6 and iNOS) and oxidative stress and increased the gene expression of insulin signaling pathway (Glut4 and p-IRβ).Conclusion Palmitateinduced insulin resistance is accompanied by elevated pro-inflammatory cytokines,oxidative stress and impaired gene expression of insulin signaling pathway.And DHA decreases inflammation and oxidative stress and increases glucose uptake in C2C12 cells.Thus DHA attenuates palmitate-induced insulin resistance.
