自然衰老与半乳糖衰老模型大鼠心肌与非酶糖基化相关性研究

目的以非酶糖基化和自由基学说探讨心肌老化的发生机制。方法用D-半乳糖制作老化模型与自然衰老组及成年对照组SD大鼠相比较,观察电镜下心肌超微结构的改变及心肌内AGEs含量,抗氧化指标的变化,及各组线粒体DNA(mtDNA)的缺失率。结果2组衰老组糖基化终末期产物(AGEs)、mtDNA缺失率及丙二醛(MDA)均较成年对照组显著增高,过氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)在2组衰老模型较成年对照组显著降低,自然老化和半乳糖老化病理都表现为肌细胞肿大,脂褐素沉积,线粒体和肌质网等膜结构明显损伤。结论心肌的老化与非酶糖基化(NEG)相关,而其诱导自由基的损伤,导致心肌细胞的凋亡。

Relationship between the glycation and myocardial aging in the rat of natural senility and aging by D-galactose

Objective To investigate the mechanisms of nonenzymatic glycosylation inducing myocardial aging and free radical theory.Methods Using D-galactose aging model and nature aging model to compare with control group,the myocardial histopathological changes under electron microscope,the contents of AGEs and oxidative mark in the cardiac tissue were observed.The mitochondrial DNA(mtDNA)deletion level in cardiac cell was examined using polymerase chain reaction(PCR).Results(1)The contents of AGEs,mtDNA,SOD and GSH-PX in the myocardial tissue of nature and D-galac-tose aging groups were significantly increased.The MDAlevel in the cardiac tissue was higher than that of the control group.(2)The electron microscope showed that myocyte swell,lipofusin deposit and the membrane structure of mitochondria and sarcoplasmic reticulum were damaged in the nature aging and D-galactose aging groups.Conclusions The myocardial aging is relative with the nonenzymatic glycosylation which induces free radical damage and myocardial cell apoptosis.