中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2014年
10期
1902-1904,1909
,共4页
戴红良%黄雷%贾桂枝%梁春光%李昕%戚春玲
戴紅良%黃雷%賈桂枝%樑春光%李昕%慼春玲
대홍량%황뢰%가계지%량춘광%리흔%척춘령
左卡尼汀%心肌细胞%氧化性应激%NFATc3蛋白
左卡尼汀%心肌細胞%氧化性應激%NFATc3蛋白
좌잡니정%심기세포%양화성응격%NFATc3단백
L-carnitine%Cardiomyocytes%Oxidative stress%NFATc3 protein
目的:探讨在过氧化氢( H2 O2)刺激下,左卡尼汀对心肌细胞内胞浆活化 T 细胞核因子3(NFATc3)的表达及分布的影响。方法:以200μmol/L H2O2刺激心肌细胞12 h建立氧化应激模型。在药物处理组,于氧化刺激前30 min加入左卡尼汀及钙调神经磷酸酶( CaN)特异性抑制剂环孢素A( CsA)。待刺激完成后,利用蛋白质免疫印迹法检测细胞内总NFATc3,以及胞浆内和胞核内NFATc3的水平,并以免疫荧光法检测NFATc3在细胞中的分布状况。结果:H2 O2刺激不影响心肌细胞NFATc3的表达,但可诱导其由胞浆至胞核的转位。左卡尼汀预处理可以显著抑制NFATc3的核转位。结论:左卡尼汀可通过抑制NFATc3的核转位发挥其抗氧化应激损伤的作用。
目的:探討在過氧化氫( H2 O2)刺激下,左卡尼汀對心肌細胞內胞漿活化 T 細胞覈因子3(NFATc3)的錶達及分佈的影響。方法:以200μmol/L H2O2刺激心肌細胞12 h建立氧化應激模型。在藥物處理組,于氧化刺激前30 min加入左卡尼汀及鈣調神經燐痠酶( CaN)特異性抑製劑環孢素A( CsA)。待刺激完成後,利用蛋白質免疫印跡法檢測細胞內總NFATc3,以及胞漿內和胞覈內NFATc3的水平,併以免疫熒光法檢測NFATc3在細胞中的分佈狀況。結果:H2 O2刺激不影響心肌細胞NFATc3的錶達,但可誘導其由胞漿至胞覈的轉位。左卡尼汀預處理可以顯著抑製NFATc3的覈轉位。結論:左卡尼汀可通過抑製NFATc3的覈轉位髮揮其抗氧化應激損傷的作用。
목적:탐토재과양화경( H2 O2)자격하,좌잡니정대심기세포내포장활화 T 세포핵인자3(NFATc3)적표체급분포적영향。방법:이200μmol/L H2O2자격심기세포12 h건립양화응격모형。재약물처리조,우양화자격전30 min가입좌잡니정급개조신경린산매( CaN)특이성억제제배포소A( CsA)。대자격완성후,이용단백질면역인적법검측세포내총NFATc3,이급포장내화포핵내NFATc3적수평,병이면역형광법검측NFATc3재세포중적분포상황。결과:H2 O2자격불영향심기세포NFATc3적표체,단가유도기유포장지포핵적전위。좌잡니정예처리가이현저억제NFATc3적핵전위。결론:좌잡니정가통과억제NFATc3적핵전위발휘기항양화응격손상적작용。
AIM: To explore the effect of L-carnitine on nuclear factor of activated T-cells, cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation.METHODS: Primary cultured neonatal rat myocardial cells were stimulated by H2 O2 at concentration of 200μmol/L for 12 h to induce oxidative stress injury.In treatment group, L-carni-tine and cyclosporin A ( CsA) , a specific inhibitor of calcineurin ( CaN) , were administered 30 min prior to H2 O2 stimula-tion.After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting.The method of immunofluoresence was used to evaluate the distribution of NFATc3.RESULTS: H2 O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment.CONCLUSION:L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.