福建医科大学学报
福建醫科大學學報
복건의과대학학보
JOURNAL OF FUJIAN MEDICAL UNIVERSITY
2014年
4期
222-226
,共5页
王丽静%陈丽云%刘晓红%陈洲%刘礼斌
王麗靜%陳麗雲%劉曉紅%陳洲%劉禮斌
왕려정%진려운%류효홍%진주%류례빈
胰高血糖素样肽1%内皮 ,血管%脐静脉%细胞凋亡%氧化性应激%细胞 ,培养的
胰高血糖素樣肽1%內皮 ,血管%臍靜脈%細胞凋亡%氧化性應激%細胞 ,培養的
이고혈당소양태1%내피 ,혈관%제정맥%세포조망%양화성응격%세포 ,배양적
glucagon-like peptide 1%endothelium,vascular%umbilical veins%apoptosis%oxidative stress%cells,cultured
目的:探讨胰高血糖素样肽-1(GLP-1)对高糖培养的原代人脐静脉内皮细胞(HUVECs)氧化应激情况的影响。方法体外分离、培养原代人 HUVECs ,分为对照组、高糖组(30 mmol/L )及 GLP-1预处理组(GLP-1100 nmol/L预处理1 h后30 mmol/L高糖培养)。检测细胞上清乳酸脱氢酶(LDH)漏出量,进行细胞毒性作用定量分析;化学发光法检测细胞内活性氧族(ROS )水平、黄嘌呤氧化酶法检测超氧化物歧化酶(SOD )活力了解细胞内氧化应激状态。结果(1)GLP-1可以改善高糖环境对人脐静脉内皮细胞的毒性作用,高糖组LDH漏出量为对照组的1.8倍,GLP-1预处理组的LDH漏出量为对照组的1.3倍(P<0.05)。(2)高糖组细胞内ROS荧光强度较对照组增强1倍以上,而GLP-1预处理组ROS荧光强度可抑制至对照组水平(P<0.05);与对照组比较,高糖组细胞内SOD酶活性无明显改变;但与高糖组比较,GLP-1预处理组SOD酶活性升高了64.64%(P<0.05)。结论 GLP-1可以改善高糖对 HUVECs的细胞毒性作用,其机制可能是通过减轻细胞氧化应激来实现的。
目的:探討胰高血糖素樣肽-1(GLP-1)對高糖培養的原代人臍靜脈內皮細胞(HUVECs)氧化應激情況的影響。方法體外分離、培養原代人 HUVECs ,分為對照組、高糖組(30 mmol/L )及 GLP-1預處理組(GLP-1100 nmol/L預處理1 h後30 mmol/L高糖培養)。檢測細胞上清乳痠脫氫酶(LDH)漏齣量,進行細胞毒性作用定量分析;化學髮光法檢測細胞內活性氧族(ROS )水平、黃嘌呤氧化酶法檢測超氧化物歧化酶(SOD )活力瞭解細胞內氧化應激狀態。結果(1)GLP-1可以改善高糖環境對人臍靜脈內皮細胞的毒性作用,高糖組LDH漏齣量為對照組的1.8倍,GLP-1預處理組的LDH漏齣量為對照組的1.3倍(P<0.05)。(2)高糖組細胞內ROS熒光彊度較對照組增彊1倍以上,而GLP-1預處理組ROS熒光彊度可抑製至對照組水平(P<0.05);與對照組比較,高糖組細胞內SOD酶活性無明顯改變;但與高糖組比較,GLP-1預處理組SOD酶活性升高瞭64.64%(P<0.05)。結論 GLP-1可以改善高糖對 HUVECs的細胞毒性作用,其機製可能是通過減輕細胞氧化應激來實現的。
목적:탐토이고혈당소양태-1(GLP-1)대고당배양적원대인제정맥내피세포(HUVECs)양화응격정황적영향。방법체외분리、배양원대인 HUVECs ,분위대조조、고당조(30 mmol/L )급 GLP-1예처리조(GLP-1100 nmol/L예처리1 h후30 mmol/L고당배양)。검측세포상청유산탈경매(LDH)루출량,진행세포독성작용정량분석;화학발광법검측세포내활성양족(ROS )수평、황표령양화매법검측초양화물기화매(SOD )활력료해세포내양화응격상태。결과(1)GLP-1가이개선고당배경대인제정맥내피세포적독성작용,고당조LDH루출량위대조조적1.8배,GLP-1예처리조적LDH루출량위대조조적1.3배(P<0.05)。(2)고당조세포내ROS형광강도교대조조증강1배이상,이GLP-1예처리조ROS형광강도가억제지대조조수평(P<0.05);여대조조비교,고당조세포내SOD매활성무명현개변;단여고당조비교,GLP-1예처리조SOD매활성승고료64.64%(P<0.05)。결론 GLP-1가이개선고당대 HUVECs적세포독성작용,기궤제가능시통과감경세포양화응격래실현적。
Objective To investigate the effects and mechanism of glucagon-like peptide-1 (GLP-1) on high glucose-induced human umbilical vein endothelial cells (HUVECs) oxidative stress . Methods HUVECs was isolated and cultured in vitro ,randomly divided into control group ,high glucose (30 mmol/L) group and GLP-1 group (100 nmol/L GLP-1+ high glucose) . Endothelial toxicity was evaluated by lactate dehydrogenase (LDH) method . Intracellular reactive oxygen species (ROS) produc-tion and activity of superoxide dismutase (SOD) reflects the oxidative stress state in the cell . Fluores-cence enzyme-labeled instrument was used to detect the production of ROS . The activity of SOD was de-tected by xanthine oxidase method . Results (1)GLP-1 could reduce toxicity of high glucose . After high glucose trestment ,the ratio of LDH leakage was markly increased to 1 .8 times of the control group . <br> However ,the ratio of LDH leakage in cells pre-treated with 100 nmol/L GLP-1 significantly decreased to 1 .3 times of the control group(P<0 .05) . (2)Comparing with control group ,ROS production was in-creased more than 1 times(P<0 .05) and the activity of SOD had no significant changes in high glucose group . After GLP-1 pretreatment ,ROS was lowered to the level of control group and activity of SOD was increased by 64 .64% (P< 0 .05) . Conclusions GLP-1 has a direct protective effect on HUVECs function under high glucose condition ,w hich is probably related to the mitigation of oxidative stress .