Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reporte...Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.展开更多
目的:探讨高胆固醇血症(Hypercholesterolemia,HTC)对wistar大鼠主动脉基因组DNA总甲基化水平及总甲基转移酶活力的影响并比较高同型半胱氨酸血症(Hyperhomocysteinemia,HHCY)和HTC在影响主动脉基因组DNA总甲基化水平、总甲基转移酶活...目的:探讨高胆固醇血症(Hypercholesterolemia,HTC)对wistar大鼠主动脉基因组DNA总甲基化水平及总甲基转移酶活力的影响并比较高同型半胱氨酸血症(Hyperhomocysteinemia,HHCY)和HTC在影响主动脉基因组DNA总甲基化水平、总甲基转移酶活力之间的差异。方法:将wistar大鼠33只,随机分3组:对照组、蛋氨酸组、高胆固醇组,每组11只。对照组给予普通大鼠饲料,其余各组给予相应的配方饲料。持续喂养3个月后心脏取血检测血清同型半胱氨酸(Homocysteine,Hcy)、总胆固醇(Total cholesterol,TC)等相关指标。提取主动脉基因组DNA检测基因组DNA总甲基化水平、提取主动脉核蛋白检测基因组DNA总甲基转移酶活力。结果:经多个样本均数间的多重比较(Dunnett-t检验):高胆固醇组大鼠的血清TC水平明显高于对照组和蛋氨酸组,且差异有统计学意义(P<0.05),血清中甘油三酯(Triglyceride,TG)、低密度脂蛋白胆固醇(Low density lipoprotein-cholesterol,LDL-C)和高密度脂蛋白胆固醇(High density lipoprotein-cholesterol,HDL-C),差异无统计学意义(P>0.05)。蛋氨酸组大鼠血清Hcy水平明显高于对照组及高胆固醇组,且差异有统计学意义(P<0.05)。HHCY和HTC均增加基因组DNA总甲基转移酶活力,可促使基因组DNA去甲基化,与对照组相比,各组均具有统计学意义(P<0.05),但两组之间差异无显著性。结论:HTC降低大鼠主动脉基因组DNA总甲基化水平可能是HTC导致动脉粥样硬化发病重要机制之一,且HHCY和HTC在影响基因组DNA低甲基化之间的差异无显著。展开更多
文摘Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. At present, the main therapeutic provision is to supply vitamin B 6, B 12 and folic acids, and the toxic and ill effect have been reported. Homocysteine, taurine, hydrogen sulfide and metallothionein are metabolic products from methionine. Homocysteine induces necrosis of endothelium, proliferation of vascular smooth muscle cells, proliferation and activation of vascular fibroblast cells and mitochondrial structural destruction and dysfunction of myocardium cells. Taurine, an end metabolic product of homocysteine, obviously reduces cardiovascular injury induced by homocysteine. The possible mechanism of antagonism by reducing oxidative stress and endoplasmic reticulum stress has been proved. Hydrogen sulfide, another end metabolic product of homocysteine, obviously reducing cardiovascular injury of homocysteine by scavenging oxidative radicals has been found. Metallothionein a derivant production of homocysteine metabolism, antagonism to homocysteine injury to cardiovascular system been discussed. Homocysteine, taurine, hydrogen sulfide and metallothionein, as a metabolic product of methionine, interactive antagonism and interactive biological influence have been reviewed. Induced endogenous or exogenous supply of taurine, hydrogen sulfide and metallothionein might resist cardiovascular injury induced by hyperhomocysteinemia. According to the methionine metabolic cycle, using endogenous antagonistic substances might be a new clinical preventive and treatment target of homocystinemia.
文摘目的:探讨高胆固醇血症(Hypercholesterolemia,HTC)对wistar大鼠主动脉基因组DNA总甲基化水平及总甲基转移酶活力的影响并比较高同型半胱氨酸血症(Hyperhomocysteinemia,HHCY)和HTC在影响主动脉基因组DNA总甲基化水平、总甲基转移酶活力之间的差异。方法:将wistar大鼠33只,随机分3组:对照组、蛋氨酸组、高胆固醇组,每组11只。对照组给予普通大鼠饲料,其余各组给予相应的配方饲料。持续喂养3个月后心脏取血检测血清同型半胱氨酸(Homocysteine,Hcy)、总胆固醇(Total cholesterol,TC)等相关指标。提取主动脉基因组DNA检测基因组DNA总甲基化水平、提取主动脉核蛋白检测基因组DNA总甲基转移酶活力。结果:经多个样本均数间的多重比较(Dunnett-t检验):高胆固醇组大鼠的血清TC水平明显高于对照组和蛋氨酸组,且差异有统计学意义(P<0.05),血清中甘油三酯(Triglyceride,TG)、低密度脂蛋白胆固醇(Low density lipoprotein-cholesterol,LDL-C)和高密度脂蛋白胆固醇(High density lipoprotein-cholesterol,HDL-C),差异无统计学意义(P>0.05)。蛋氨酸组大鼠血清Hcy水平明显高于对照组及高胆固醇组,且差异有统计学意义(P<0.05)。HHCY和HTC均增加基因组DNA总甲基转移酶活力,可促使基因组DNA去甲基化,与对照组相比,各组均具有统计学意义(P<0.05),但两组之间差异无显著性。结论:HTC降低大鼠主动脉基因组DNA总甲基化水平可能是HTC导致动脉粥样硬化发病重要机制之一,且HHCY和HTC在影响基因组DNA低甲基化之间的差异无显著。
