中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2012年
34期
2406-2409
,共4页
门莉莉%许静宜%杜建玲%宋桂荣%许琳%杨郁%周海成%邢倩
門莉莉%許靜宜%杜建玲%宋桂榮%許琳%楊鬱%週海成%邢倩
문리리%허정의%두건령%송계영%허림%양욱%주해성%형천
β-淀粉样肽%糖尿病%2型%血管内皮细胞%氧化应激
β-澱粉樣肽%糖尿病%2型%血管內皮細胞%氧化應激
β-정분양태%당뇨병%2형%혈관내피세포%양화응격
Amyloid beta-peptides%Diabetcs mellitus%type 2%Vascular endothelial cells%Oxidative stress
目的 探讨糖尿病(DM)血管内皮细胞损伤与β淀粉样肽(Aβ)的相关性.方法 选取2型糖尿病患者(DM组)和健康对照(HC组)各10例,利用其血清对人脐静脉内皮细胞株(HUVEC)进行干预,同时胎牛血清作为对照组(FBS组),检测干预72 h时内皮细胞生存率,干预0.5、3、72 h时上清液中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、Aβ40以及Aβ42的含量.结果 DM患者Aβ40较健康对照者明显升高(P<0.01);上清液中Aβ40[0.5、3、72 h时,DM 组分别为( 163 ±64)、(207 ±69)、( 286±75) ng/L,HC组分别为(146 ±76)、(154 ±75)、(161 ±72)ng/L]以及Aβ42的水平[0.5、3、72 h时,DM组分别为(48 ±46)、(54±43)、(79 ±44) ng/L,HC组分别为(41±12)、(44±16)、(49 ±12) ng/L],组别与干预时间均有交互作用(P<0.05).HC与FBS 组随着干预时间的延长,DM组SOD和NO水平,呈下降趋势,72 h时最低,而HC和FBS组呈上升趋势,72 h时最高;Pearson相关分析显示,在干预72 h时SOD与Aβ40和Aβ42呈负相关(r=-0.482、-0.422,P<0.05);MDA与Aβ40和Aβ42呈正相关(r=0.418、0.833,P<0.01).结论 DM血管内皮细胞氧化应激损伤与Aβ40、Aβ42有关.
目的 探討糖尿病(DM)血管內皮細胞損傷與β澱粉樣肽(Aβ)的相關性.方法 選取2型糖尿病患者(DM組)和健康對照(HC組)各10例,利用其血清對人臍靜脈內皮細胞株(HUVEC)進行榦預,同時胎牛血清作為對照組(FBS組),檢測榦預72 h時內皮細胞生存率,榦預0.5、3、72 h時上清液中超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮(NO)、Aβ40以及Aβ42的含量.結果 DM患者Aβ40較健康對照者明顯升高(P<0.01);上清液中Aβ40[0.5、3、72 h時,DM 組分彆為( 163 ±64)、(207 ±69)、( 286±75) ng/L,HC組分彆為(146 ±76)、(154 ±75)、(161 ±72)ng/L]以及Aβ42的水平[0.5、3、72 h時,DM組分彆為(48 ±46)、(54±43)、(79 ±44) ng/L,HC組分彆為(41±12)、(44±16)、(49 ±12) ng/L],組彆與榦預時間均有交互作用(P<0.05).HC與FBS 組隨著榦預時間的延長,DM組SOD和NO水平,呈下降趨勢,72 h時最低,而HC和FBS組呈上升趨勢,72 h時最高;Pearson相關分析顯示,在榦預72 h時SOD與Aβ40和Aβ42呈負相關(r=-0.482、-0.422,P<0.05);MDA與Aβ40和Aβ42呈正相關(r=0.418、0.833,P<0.01).結論 DM血管內皮細胞氧化應激損傷與Aβ40、Aβ42有關.
목적 탐토당뇨병(DM)혈관내피세포손상여β정분양태(Aβ)적상관성.방법 선취2형당뇨병환자(DM조)화건강대조(HC조)각10례,이용기혈청대인제정맥내피세포주(HUVEC)진행간예,동시태우혈청작위대조조(FBS조),검측간예72 h시내피세포생존솔,간예0.5、3、72 h시상청액중초양화물기화매(SOD)、병이철(MDA)、일양화담(NO)、Aβ40이급Aβ42적함량.결과 DM환자Aβ40교건강대조자명현승고(P<0.01);상청액중Aβ40[0.5、3、72 h시,DM 조분별위( 163 ±64)、(207 ±69)、( 286±75) ng/L,HC조분별위(146 ±76)、(154 ±75)、(161 ±72)ng/L]이급Aβ42적수평[0.5、3、72 h시,DM조분별위(48 ±46)、(54±43)、(79 ±44) ng/L,HC조분별위(41±12)、(44±16)、(49 ±12) ng/L],조별여간예시간균유교호작용(P<0.05).HC여FBS 조수착간예시간적연장,DM조SOD화NO수평,정하강추세,72 h시최저,이HC화FBS조정상승추세,72 h시최고;Pearson상관분석현시,재간예72 h시SOD여Aβ40화Aβ42정부상관(r=-0.482、-0.422,P<0.05);MDA여Aβ40화Aβ42정정상관(r=0.418、0.833,P<0.01).결론 DM혈관내피세포양화응격손상여Aβ40、Aβ42유관.
Objective To explore the relationship of the impairment of human umbilical vein endothelial cell (HUVEC) with amyloid-β.Methods HUVECs were cultured in the serum of patients with type 2 diabetes mellitus (DM) or serum of healthy control (HC),while fetal bovine serum (FBS) was used as a negative control.The proliferative activity of HUVEC were assessed by thiazoyl blue tetrazolium bromide (MTT) after 72 h. The supernatant concentrations of superoxide dismutase (SOD),maleic dialdehyde (MDA),nitric oxide (NO),amyloid-β40 (Aβ40) and Aβ42 were measured after 0.5,3 and 72 h respectively.Results Glycosylated hemoglobin values,fasting plasma glucose and fasting plasma Aβ40 concentrations of diatbetic patients were higher than those of healthy counterparts ( P < 0.01 ).Proliferativeactivity of HUVECs in group DM were significantly lower than that of group HC.Both group and the time of intervention had crossover effects on the levels of MDA,SOD,NO and Aβ40 ( ( 163 ± 64 ),(207 ±69 ),(286 ±75) ng/L in group DM; (146 ±76),(154 ±75),(161 ±72) ng/L in group HC after 0.5,3 and 72 h,P <0.05) and Aβ42 ( (48 ±46),(54 ±43),(79 ±44) ng/L in group DM; (41 ± 12),(44 ±16),(48 ± 12) ng/L in group HC after 0.5,3 and 72 h,P <0.05).With the elongating time of intervention,the levels of SOD and NO decreased significantly in group DM and reached the lowest after 72 h while increased significantly in groups HC and FBS and peaked after 72 h.The concentrations of MDA,Aβ40 and Aβ42 increased significantly in all three groups while the fastest and marked increments were found in group DM ( P < 0.01 ).Pearson correlation analysis showed that SOD was negatively correlated with Aβ40 (r=-0.482,P=0.02)and Aβ42 (r=-0.422,P=0.02) while MDA positively with Aβ40 (r=0.418,P<0.05) and Aβ42 (r=0.833,P<0.05) after72 h.Conclusion Oxidative stress of vascular endothelial cells may be correlated with Aβ40 and Aβ42 in diabetes.