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目的比较正常和衰竭心肌组织相关酶活性及β_3肾上腺素能受体(β_3受体)、过氧化物酶体增生物激活受体α(PPARα受体)基因和蛋白表达的变化,探讨心力衰竭(心衰)代谢重构的可能机制。方法选取20例瓣膜置换术的心衰患者和6例意外伤亡健康者心肌组织,检测心肌游离脂肪酸(FFA)、琥珀酸脱氢酶(sDH)和 ATP 酶活力。应用 RT-PCR 和 Western-blot 方法分别检测心肌组织β_3受体和 PPARα受体 mRNA 和蛋白表达。结果衰竭心肌 FFA 含量明显增加(P<0.01);SDH、Na~+-K~+-ATP 酶和 Ca~(2+)-Mg~(2+)-ATP 酶活性则显著降低(P<0.01,P<0.05和 P<0.01)。衰竭心肌β_3受体 mRNA 和蛋白表达明显高于正常心肌;而 PPARα受体表达则显著低于正常心肌。结论心衰时存在代谢重构,表现为心肌代谢底物发生转变,代谢相关酶活性下降等;β_3受体和 PPARα受体在衰竭心肌分别上调和下调,可能参与心肌组织代谢重构。
Objective To compare the changes of enzyme activity and the gene and protein expression of β 3 adrenergic receptor (β 3 receptor) and peroxisome proliferator activated receptor α (PPAR α receptor) in normal and failing myocardium, Heart failure) possible mechanisms of metabolic remodeling. Methods Twenty cases of heart failure and 6 cases of uninjured casualty heart valve replacement were enrolled in this study. Myocardial free fatty acid (FFA), succinate dehydrogenase (sDH) and ATPase activity were measured. The mRNA and protein expression of β 3 receptor and PPAR α receptor in myocardium were detected by RT-PCR and Western-blot respectively. Results FFA content in the exhausted myocardium was significantly increased (P <0.01). The activities of SDH, Na ~ + -K ~ + -ATPase and Ca ~ (2 +) - Mg ~ (2 + , P <0.05 and P <0.01). The expression of β 3 receptor mRNA and protein in failing myocardium was significantly higher than that in normal myocardium while the expression of PPARα receptor was significantly lower than that in normal myocardium. Conclusions Metabolic remodeling exists in heart failure, which manifests as the change of myocardial metabolic substrates and the decrease of metabolic enzyme activities. The β 3 receptor and PPAR α receptor are up-regulated and down-regulated respectively in myocardial failure, which may be involved in myocardial remodeling.