中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2012年
11期
954-958
,共5页
谭超超%唐建华%卢永娟%李娜
譚超超%唐建華%盧永娟%李娜
담초초%당건화%로영연%리나
磷脂酶类%内皮,血管%动脉粥样硬化
燐脂酶類%內皮,血管%動脈粥樣硬化
린지매류%내피,혈관%동맥죽양경화
Phospholipases%Endothelium,vascular%Atherosclerosis
目的 探讨糖基化磷脂酰肌醇特异性磷脂酶D(GPI-PLD)在动脉粥样硬化病理生理过程中的作用及其机制. 方法 分别收集102例冠心病患者和121例健康者外周血,测定其外周血GPI-PLD酶活性及其单个核细胞GPI-PLD mRNA表达.构建高表达GPI-PLD基因HUVEC细胞模型,并设立空白组和对照组,进行ox-LDL诱导,观察各组内皮细胞功能及生物学特性的改变.结果 冠心病患者和健康者其外周血GPI-PLD酶活性分别为31.80±4.21和44.32±4.50,单个核细胞GPI-PLD mRNA表达比值分别是0.92±0.16和1.53±0.14;冠心病患者组外周血GPI-PLD酶活性(t=21.31,P＜0.01)及其mRNA表达(t=30.36,P＜0.01),较健康者组分别减少28.2％和39.9％.ox-LDL诱导的各组细胞,高表达GPI-PLD细胞模型组细胞表面黏附单核细胞数、内皮素1、活性氧、丙二醛及凋亡率均低于空白组[29.59±1.40、3.51±0.45、(50.63±4.22) ng/L、0.043±0.011、(3.32±0.44) nmol/L比41.39±2.15、10.57±1.12、(59.35±4.45) ng/L、0.052±0.011、(5.01±0.69) nmol/L]和对照组[42.68±2.45、9.92±1.03、(61.11±4.12) ng/L、0.051±0.007、(4.89±0.71)nmol/L],而一氧化氮含量高于空白组[(29.88±1.37 μmol/L比(21.76±1.02) μmol/L]和对照组(23.43±0.85) μmol/L. 结论 GPI-PLD基因在冠心病患者中低表达,稳定高表达GPI-PLD有助于血管内皮细胞损伤的修复,有助于阻止动脉粥样硬化的发生和发展.
目的 探討糖基化燐脂酰肌醇特異性燐脂酶D(GPI-PLD)在動脈粥樣硬化病理生理過程中的作用及其機製. 方法 分彆收集102例冠心病患者和121例健康者外週血,測定其外週血GPI-PLD酶活性及其單箇覈細胞GPI-PLD mRNA錶達.構建高錶達GPI-PLD基因HUVEC細胞模型,併設立空白組和對照組,進行ox-LDL誘導,觀察各組內皮細胞功能及生物學特性的改變.結果 冠心病患者和健康者其外週血GPI-PLD酶活性分彆為31.80±4.21和44.32±4.50,單箇覈細胞GPI-PLD mRNA錶達比值分彆是0.92±0.16和1.53±0.14;冠心病患者組外週血GPI-PLD酶活性(t=21.31,P＜0.01)及其mRNA錶達(t=30.36,P＜0.01),較健康者組分彆減少28.2％和39.9％.ox-LDL誘導的各組細胞,高錶達GPI-PLD細胞模型組細胞錶麵黏附單覈細胞數、內皮素1、活性氧、丙二醛及凋亡率均低于空白組[29.59±1.40、3.51±0.45、(50.63±4.22) ng/L、0.043±0.011、(3.32±0.44) nmol/L比41.39±2.15、10.57±1.12、(59.35±4.45) ng/L、0.052±0.011、(5.01±0.69) nmol/L]和對照組[42.68±2.45、9.92±1.03、(61.11±4.12) ng/L、0.051±0.007、(4.89±0.71)nmol/L],而一氧化氮含量高于空白組[(29.88±1.37 μmol/L比(21.76±1.02) μmol/L]和對照組(23.43±0.85) μmol/L. 結論 GPI-PLD基因在冠心病患者中低錶達,穩定高錶達GPI-PLD有助于血管內皮細胞損傷的脩複,有助于阻止動脈粥樣硬化的髮生和髮展.
목적 탐토당기화린지선기순특이성린지매D(GPI-PLD)재동맥죽양경화병리생리과정중적작용급기궤제. 방법 분별수집102례관심병환자화121례건강자외주혈,측정기외주혈GPI-PLD매활성급기단개핵세포GPI-PLD mRNA표체.구건고표체GPI-PLD기인HUVEC세포모형,병설립공백조화대조조,진행ox-LDL유도,관찰각조내피세포공능급생물학특성적개변.결과 관심병환자화건강자기외주혈GPI-PLD매활성분별위31.80±4.21화44.32±4.50,단개핵세포GPI-PLD mRNA표체비치분별시0.92±0.16화1.53±0.14;관심병환자조외주혈GPI-PLD매활성(t=21.31,P＜0.01)급기mRNA표체(t=30.36,P＜0.01),교건강자조분별감소28.2％화39.9％.ox-LDL유도적각조세포,고표체GPI-PLD세포모형조세포표면점부단핵세포수、내피소1、활성양、병이철급조망솔균저우공백조[29.59±1.40、3.51±0.45、(50.63±4.22) ng/L、0.043±0.011、(3.32±0.44) nmol/L비41.39±2.15、10.57±1.12、(59.35±4.45) ng/L、0.052±0.011、(5.01±0.69) nmol/L]화대조조[42.68±2.45、9.92±1.03、(61.11±4.12) ng/L、0.051±0.007、(4.89±0.71)nmol/L],이일양화담함량고우공백조[(29.88±1.37 μmol/L비(21.76±1.02) μmol/L]화대조조(23.43±0.85) μmol/L. 결론 GPI-PLD기인재관심병환자중저표체,은정고표체GPI-PLD유조우혈관내피세포손상적수복,유조우조지동맥죽양경화적발생화발전.
Objective To investigate the effect of glycosylphosphatidylinositol specific phospholipase D (GPI-PLD) on artherosclerosis.Methods The GPI-PLD activities and mononuclear cells GPI-PLD gene mRNA expression was detected in 102 patients with coronary artery disease and 121 healthy adult.The GPI-PLD highly expressing cell model was constructed and induced by ox-LDL,the HUVEC and HUVEC transfected with pcDNA3.1(+) as blank and control group,respectively.Before and after the induction,the change of cellular function and biological features was detected.Results The peripheral blood GPI-PLD activity of patients with coronary heart disease and normal control were 31.80±4.21 and 44.32±4.50,and the IA ratio of GPI-PLD mRNA expression of mononuclear cells were 0.92±0.16 and 1.53±0.14,respectively.The activity of GPI-PLD and mRNA expression in patients with coronary artery disease were decreased up to 28.2％ (t=21.31,P＜0.01) and 39.9％ (t=30.36,P＜0.01) as compared with healthy control.The adhesion cells,ET-1,reactive oxygen,malondialdehyde (MDA) and the apoptosis rate of GPI-PLD overexpressing HUVEC were lower as compared with blank [29.59=1.40,3.51 ± 0.45,(50.63 ±4.22) ng/L,0.043±0.011,(3.32±0.44) nmol/L vs.41.39±2.15,10.57±1.12,(59.35±4.45)ng/L,0.052±0.011,(5.01±0.69) nmol/L],and as compared with control [42.68±2.45,9.92±1.03,(61.11±4.12) ng/L,0.051±0.007,(4.89±0.71) nmol/l] after inducing by ox-LDL; while the level of nitrogen noxidium (NO) was higher than blank [(29.88± 1.37)μmol/L vs.(21.76±1.02)μmol/L] and control(23.43±0.85)μmol/L groups.Conclusions The expression and activity of GPI-PLD in patients with coronary artery disease are lower than health people.Stable high expression of GPI-PLD is beneficial to vascular endothelial cell injury repairment and prevent the occurrence and development of atherosclerosis.
