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束缚应激后大鼠心脏PPARβ、M-CPT-I及GLUT-4 mRNA的变化 被引量:2

Effect of restraint stress on the expressions of PPARβ,M-CPT-I and GLUT-4 mRNA in the myocardium of rats
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摘要 目的:观察束缚应激后大鼠心肌PPARβ、M-CPT-I和GLUT-4的mRNA表达变化。方法:健康雄性Wister大鼠,分为正常对照组(C)、束缚1周组(R1)、束缚2周组(R2)和束缚4周组(R4)。心肌PPARβ、M-CPT-I和GLUT-4的mR-NA表达水平用RT-PCR方法检测。结果:与正常对照组大鼠相比,束缚应激1、2、4周大鼠心肌M-CPT-I mRNA水平明显升高(R2组P<0.05,其余P<0.01),GLUT-4 mRNA水平明显降低(P<0.01),PPARβ变化不明显。结论:束缚应激后可能存在大鼠心肌脂肪酸代谢的增加和葡萄糖代谢降低。PPARβ对束缚应激大鼠心肌能量代谢的影响较小。 Objective: To observe the effect of restraint stress on the expressions of peroxisome proliferator-activated receptor β(PPARβ),muscle carnitine palmitoyl transferase-I(M-CPT-I) and glucose translator-4(GLUT-4) mRNA in the myocardium of rats.Methods: Forty-eight Wistar rats were divided into control group,1-week(R1),2-week(R2) and 4-week(R4) restraint stress group.The expressions of PPARβ,M-CPT-I and GLUT-4 mRNA in the myocardium were detected by RT-PCR.Results: Compared with control group,M-CPT-I mRNA was significantly higher(P〈0.05),GLUT-4 mRNA was significantly lower(P〈0.01),while the PPARβ mRNA has no significant change in the myocardium of rats of the R1,R2 or R4 group(P〉0.05).Conclusion: Restraint stress may increase the fatty acid oxidation and decrease the glucose oxidation.The PPARβ may not involve in the regulation of energy metabolism in the heart under restraint stress.
出处 《西北国防医学杂志》 CAS 2010年第2期99-101,共3页 Medical Journal of National Defending Forces in Northwest China
基金 国家自然科学基金资助项目(30872713)
关键词 束缚应激 心肌 过氧化体增殖物激活型受体β 肌型肉碱棕榈酰转移酶-I 葡萄糖转运蛋白-4 Restraint stress Myocardium Peroxisome proliferator-activated receptor β Muscle carnitine palmitoyl transferase-I Glucose translator-4
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参考文献5

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  • 2Bowman RE,Ferguson D,Luine VN.Effects of chronic restraint stress and estradiol on open field activity,spatial memory and monoaminergic neurotransmitters in ovariectomized rats[J].Neuroscience,2002,113 (12):401-410.
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  • 5Lionetti V,Linke A,Chandler MP,et al.Carnitine palmitoyl transferase-I inhibition prevents ventricular remodeling and delays decompensation in pacing-induced heart failure[J].Cardiovasc Res,2005,66(3):454-461.

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