中华眼科杂志
中華眼科雜誌
중화안과잡지
Chinese Journal of Ophthalmology
2009年
3期
248-253
,共6页
肖天林%Mohammad Shoeb%Naseem H.Ansari
肖天林%Mohammad Shoeb%Naseem H.Ansari
초천림%Mohammad Shoeb%Naseem H.Ansari
糖尿病并发症%白内障%过氧化脂质类%醛类
糖尿病併髮癥%白內障%過氧化脂質類%醛類
당뇨병병발증%백내장%과양화지질류%철류
Diabetes complications%Cataract%Lipid peroxidation%Aldehydes
目的 研究脂质过氧化代谢产物4-羟基壬烯醛(HNE)在糖尿病性白内障中的代谢过程以及发病中的作用.方法 实验研究.采用两因素析因设计:处理因素为两水平(正常对照组和糖尿病组),时间因素为三水平(30、45、70 d).对于不同时期的正常与糖尿病大鼠晶状体采用下列方法进行处理:(1)使用一定晕的带有放射活性的HNE与这些晶状体一起培养,测定HNE在晶状体的代谢;(2)分光光度计法测定醛脱氢酶(ALDH)活性;(3)免疫印迹法检测ALDH和HNE-蛋白质加合物的表达.采用两因素析因设计定量资料方差分析对资料进行统计学处理.结果 HNE在正常对照组的晶状体的代谢主要是与谷胱甘肽(GSH)结合形成GS-HNE(约45%),其次为经ALDH氧化成HNA(约9.1%);但糖尿病组晶状体的HNE与GSH结合径路受到抑制,GS-HNE形成减少,与正常组相比30 d时减少约64%(F=49.59,P＜0.001);而糖尿病组晶状体的ALDH氧化径路代偿增强,HNA形成增多,70 d比30 d增多约1.7倍(F=11.51,P=0.0442).糖尿病组的晶状体ALDH活性增高,免疫印迹法显示ALDH较正常对照组增多,HNE-蛋白质加合物较对照组减少.结论糖尿病性白内障中HNE与GSH的结合径路受到抑制,而氧化径路代偿性增强,揭示了结合径路的损伤可能与白内障发生有密切关系,氧化径路的代偿增强可能对防止糖尿病性白内障的发生有一定的意义.(中华眼科杂志,2009,45:248-253)
目的 研究脂質過氧化代謝產物4-羥基壬烯醛(HNE)在糖尿病性白內障中的代謝過程以及髮病中的作用.方法 實驗研究.採用兩因素析因設計:處理因素為兩水平(正常對照組和糖尿病組),時間因素為三水平(30、45、70 d).對于不同時期的正常與糖尿病大鼠晶狀體採用下列方法進行處理:(1)使用一定暈的帶有放射活性的HNE與這些晶狀體一起培養,測定HNE在晶狀體的代謝;(2)分光光度計法測定醛脫氫酶(ALDH)活性;(3)免疫印跡法檢測ALDH和HNE-蛋白質加閤物的錶達.採用兩因素析因設計定量資料方差分析對資料進行統計學處理.結果 HNE在正常對照組的晶狀體的代謝主要是與穀胱甘肽(GSH)結閤形成GS-HNE(約45%),其次為經ALDH氧化成HNA(約9.1%);但糖尿病組晶狀體的HNE與GSH結閤徑路受到抑製,GS-HNE形成減少,與正常組相比30 d時減少約64%(F=49.59,P＜0.001);而糖尿病組晶狀體的ALDH氧化徑路代償增彊,HNA形成增多,70 d比30 d增多約1.7倍(F=11.51,P=0.0442).糖尿病組的晶狀體ALDH活性增高,免疫印跡法顯示ALDH較正常對照組增多,HNE-蛋白質加閤物較對照組減少.結論糖尿病性白內障中HNE與GSH的結閤徑路受到抑製,而氧化徑路代償性增彊,揭示瞭結閤徑路的損傷可能與白內障髮生有密切關繫,氧化徑路的代償增彊可能對防止糖尿病性白內障的髮生有一定的意義.(中華眼科雜誌,2009,45:248-253)
목적 연구지질과양화대사산물4-간기임희철(HNE)재당뇨병성백내장중적대사과정이급발병중적작용.방법 실험연구.채용량인소석인설계:처리인소위량수평(정상대조조화당뇨병조),시간인소위삼수평(30、45、70 d).대우불동시기적정상여당뇨병대서정상체채용하렬방법진행처리:(1)사용일정훈적대유방사활성적HNE여저사정상체일기배양,측정HNE재정상체적대사;(2)분광광도계법측정철탈경매(ALDH)활성;(3)면역인적법검측ALDH화HNE-단백질가합물적표체.채용량인소석인설계정량자료방차분석대자료진행통계학처리.결과 HNE재정상대조조적정상체적대사주요시여곡광감태(GSH)결합형성GS-HNE(약45%),기차위경ALDH양화성HNA(약9.1%);단당뇨병조정상체적HNE여GSH결합경로수도억제,GS-HNE형성감소,여정상조상비30 d시감소약64%(F=49.59,P＜0.001);이당뇨병조정상체적ALDH양화경로대상증강,HNA형성증다,70 d비30 d증다약1.7배(F=11.51,P=0.0442).당뇨병조적정상체ALDH활성증고,면역인적법현시ALDH교정상대조조증다,HNE-단백질가합물교대조조감소.결론당뇨병성백내장중HNE여GSH적결합경로수도억제,이양화경로대상성증강,게시료결합경로적손상가능여백내장발생유밀절관계,양화경로적대상증강가능대방지당뇨병성백내장적발생유일정적의의.(중화안과잡지,2009,45:248-253)
Objective To study the metabolism of 4-hydroxynonenal(HNE),one of lipid derived aldehydes(LDAs),in diabetic rat lens and its role in diabetic cataract formation.Methods Experimental research.A factor design was used to set up the experiment statistically upon two factors:diabetic and normal ontrol as treatment factors;day 30,45 and 70 as the time factors.Normal and diabetic rats'lenses were incubated with HNE for 2 hours.HNE metabolites in the culture media were studied by high performance liquid chromatography(HPLC).Aldehyde dehydrogenase(ALDH)activity in normal and diabetic rat lens(30,45 and 70 d after inducing of cataract)was detected by a spectrophotometer,ALDH protein and HNE protein were detected by Western Blot.All data were analyzed by the Bonferroni test using SAS 8.0 software.Results The major pathway for HNE metabolism in normal lens was conjugation with glutathione (GSH)to form GS-HNE(45%),followed by HNE's oxidation to 4-hydroxy-2-nonenoic acid(HNA)by ALDH,which accounted for approximately 9.1% of HNE.The conjugation of HNE with GSH in diabetic lens was decreased approximately 64% at day 30 compared with the controls(F=49.59,P＜0.001).The pathway of HNE oxidation by ALDH in the diabetic lens was enhanced approximately 1.7 times at day 70 compared to day 30(F=11.51,P=0.0442).A higher ALDH activity,greater amount of ALDH protein,and less amount of HNE-protein adduct were presented in diabetic rat lens.Conclusions The pathway of conjugation of HNE with GSH is inhibited in diabetic lens which may play a role in the formation of diabetic cataract.The oxidation of HNE by ALDH is a compensation process for protecting the lens against diabetic damage.(Chin J Ophthalmol,2009,45:248-253)
