中华糖尿病杂志
中華糖尿病雜誌
중화당뇨병잡지
CHINES JOURNAL OF DLABETES MELLITUS
2009年
5期
355-358
,共4页
吴晨光%王丽%方春钱%高静
吳晨光%王麗%方春錢%高靜
오신광%왕려%방춘전%고정
还原型谷胱汁肽%糖尿病肾病%氧化应激%线粒体
還原型穀胱汁肽%糖尿病腎病%氧化應激%線粒體
환원형곡광즙태%당뇨병신병%양화응격%선립체
Reduced glutathione%Diabetic nephropathy%Oxidative stress%Mitochondrial
目的 探讨还原型谷胱甘肽(reduced glutathione,GSH)对链脲佐菌素(streptozotocin,STZ)诱导的糖尿病大鼠肾脏线粒体保护及机制.方法 STZ诱导糖尿病大鼠模型,将糖尿病大鼠随机分为糖尿病非干预组(DM组)和GSH干预组(DM+GSH组),并以正常组(NC组)作对照.干预8周后,测定各组大鼠尿白蛋白排泄率(UAER)、血肌酐(SCr)、血尿素氮(BUN)水平,光镜观察肾脏组织形态学变化,检测血清和肾皮质中丙二醛(MDA)、超氧化物歧化酶(SOD)的含量以及各组肾脏线粒体膜电位和肿胀度的变化.结果 DM组大鼠UAER、SCr、BUN较NC组显著升高(均P＜0.05),肾脏组织发生糖尿病肾病病理改变,血清MDA(μmol/L)和肾皮质中MDA(μmol/g)显著升高(5.59±1.03 vs 2.97±0.77;4.80±0.83 vs 2.98±0.75;均P＜0.01),血清SOD(U/ml)和肾皮质中SOD(U/mg)含量显著降低(89.13±22.73 vs 124.1±9.27;46.05±10.24 vs 89.89±17.62;均P＜0.01),肾脏线粒体膜电位明显降低(495.79±124.71 vs 965.77±246.48,P＜0.05),线粒体肿胀度趋势明显减弱.与DM组相比,DM+GSH组大鼠UAER、SCr、BUN显著降低(均P＜0.05),肾脏病理形态得到一定改善.血清MDA(μmol/L)和肾皮质中MDA(μmol/g)降低(4.15±0.59 vs 5.59±1.03;3.39±0.61 vs 4.80±0.83;均P＜0.05),血清SOD(U/ml)及肾皮质中SOD(U/mg)升高(112.92±8.93 vs 89.13±22.73;83.15±16.75 vs 46.05±10.24;均P＜0.05),肾脏线粒体膜电位显著升高(715.97±188.65 vs 495.79±124.71,P＜0.05),线粒体肿胀度趋势增强.结论 还原型谷胱甘肽对STZ诱导的糖尿病大鼠肾脏病变有一定程度的保护作用,其机制可能与线粒体的功能改变有一定关系.
目的 探討還原型穀胱甘肽(reduced glutathione,GSH)對鏈脲佐菌素(streptozotocin,STZ)誘導的糖尿病大鼠腎髒線粒體保護及機製.方法 STZ誘導糖尿病大鼠模型,將糖尿病大鼠隨機分為糖尿病非榦預組(DM組)和GSH榦預組(DM+GSH組),併以正常組(NC組)作對照.榦預8週後,測定各組大鼠尿白蛋白排洩率(UAER)、血肌酐(SCr)、血尿素氮(BUN)水平,光鏡觀察腎髒組織形態學變化,檢測血清和腎皮質中丙二醛(MDA)、超氧化物歧化酶(SOD)的含量以及各組腎髒線粒體膜電位和腫脹度的變化.結果 DM組大鼠UAER、SCr、BUN較NC組顯著升高(均P＜0.05),腎髒組織髮生糖尿病腎病病理改變,血清MDA(μmol/L)和腎皮質中MDA(μmol/g)顯著升高(5.59±1.03 vs 2.97±0.77;4.80±0.83 vs 2.98±0.75;均P＜0.01),血清SOD(U/ml)和腎皮質中SOD(U/mg)含量顯著降低(89.13±22.73 vs 124.1±9.27;46.05±10.24 vs 89.89±17.62;均P＜0.01),腎髒線粒體膜電位明顯降低(495.79±124.71 vs 965.77±246.48,P＜0.05),線粒體腫脹度趨勢明顯減弱.與DM組相比,DM+GSH組大鼠UAER、SCr、BUN顯著降低(均P＜0.05),腎髒病理形態得到一定改善.血清MDA(μmol/L)和腎皮質中MDA(μmol/g)降低(4.15±0.59 vs 5.59±1.03;3.39±0.61 vs 4.80±0.83;均P＜0.05),血清SOD(U/ml)及腎皮質中SOD(U/mg)升高(112.92±8.93 vs 89.13±22.73;83.15±16.75 vs 46.05±10.24;均P＜0.05),腎髒線粒體膜電位顯著升高(715.97±188.65 vs 495.79±124.71,P＜0.05),線粒體腫脹度趨勢增彊.結論 還原型穀胱甘肽對STZ誘導的糖尿病大鼠腎髒病變有一定程度的保護作用,其機製可能與線粒體的功能改變有一定關繫.
목적 탐토환원형곡광감태(reduced glutathione,GSH)대련뇨좌균소(streptozotocin,STZ)유도적당뇨병대서신장선립체보호급궤제.방법 STZ유도당뇨병대서모형,장당뇨병대서수궤분위당뇨병비간예조(DM조)화GSH간예조(DM+GSH조),병이정상조(NC조)작대조.간예8주후,측정각조대서뇨백단백배설솔(UAER)、혈기항(SCr)、혈뇨소담(BUN)수평,광경관찰신장조직형태학변화,검측혈청화신피질중병이철(MDA)、초양화물기화매(SOD)적함량이급각조신장선립체막전위화종창도적변화.결과 DM조대서UAER、SCr、BUN교NC조현저승고(균P＜0.05),신장조직발생당뇨병신병병리개변,혈청MDA(μmol/L)화신피질중MDA(μmol/g)현저승고(5.59±1.03 vs 2.97±0.77;4.80±0.83 vs 2.98±0.75;균P＜0.01),혈청SOD(U/ml)화신피질중SOD(U/mg)함량현저강저(89.13±22.73 vs 124.1±9.27;46.05±10.24 vs 89.89±17.62;균P＜0.01),신장선립체막전위명현강저(495.79±124.71 vs 965.77±246.48,P＜0.05),선립체종창도추세명현감약.여DM조상비,DM+GSH조대서UAER、SCr、BUN현저강저(균P＜0.05),신장병리형태득도일정개선.혈청MDA(μmol/L)화신피질중MDA(μmol/g)강저(4.15±0.59 vs 5.59±1.03;3.39±0.61 vs 4.80±0.83;균P＜0.05),혈청SOD(U/ml)급신피질중SOD(U/mg)승고(112.92±8.93 vs 89.13±22.73;83.15±16.75 vs 46.05±10.24;균P＜0.05),신장선립체막전위현저승고(715.97±188.65 vs 495.79±124.71,P＜0.05),선립체종창도추세증강.결론 환원형곡광감태대STZ유도적당뇨병대서신장병변유일정정도적보호작용,기궤제가능여선립체적공능개변유일정관계.
Objective To explore the renoprotective effect of reduced glutathione on streptozotocin-induced diabetic rats and its possible mitochondrial mechanism in the kidneys.Methods After the diabetic rat models were induced by intraperitoneal injection of streptozotocin (STZ),the diabetic rats were randomly divided into non-treated group (DM),and reduced glutathione-treated group (DM + GSH).The normal non-diabetic rats were served as the control group (NC).Eight weeks later,the excretion of urinary albumin excrection rate (UAER),serum creatinine (SCr) and serum urea nitrogen (BUN) were detected.Morphological changes of the kidney were observed by optics microscope.The levels of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in serum and renal cortex were detected.Meanwhile,kidney mitochondrial membrane potential and mitochondrial swelling were measured between the different groups.Results Compared with the NC group,the excretion of UAER,SCr and BUN were significantly increased (all P ＜ 0.05),and pathological changes of diabetic nephropathy occured in the DM group.The levels of MDA in serum (μmol/L) and renal cortex (μmol/g) were significantly elevated (5.59±1.028 vs 2.97±0.77,4.80±0.83 vs 2.98±0.75,all P ＜ 0.01),and the activity of SOD in serum (U/ml) and renal cortex (U/mg) was significantly reduced in the DM group(89.13±22.73 vs 124.1±9.27,46.05±10.24 vs 89.89±17.62,all P ＜0.01).The kidney mitochondrial membrane potential was significantly decreased (495.79±124.71 vs 965.77±246.48,P ＜ 0.05),and mitochondrial swelling was weaken in the DM group.Compared with the DM group,the excretion of UAER,SCr and BUN were significantly decreased (all P ＜ 0.05),and above abnormal pathological changes were improved in the DM + GSH group.The levels of MDA in serum (μmoL/L) and renal cortex (μmol/g) were significantly reduced (4.15±0.59 vs 5.59±1.03,3.39±0.61 vs 4.80±0.83,all P＜0.05),and the activity of SOD in serum(U/ml) and renal cortex(U/mg) was significantly elevated in the DM + GSH group (112.92±8.93 vs 89.13±22.73,83.15±16.75 vs 46.05±10.24,all P＜0.05).The kidney mitochondrial membrane potential was significantly elevated (715.97±188.65 vs 495.79±124.71,P ＜ 0.05) and mitochondrial swelling was reinforced.Conclusion Reduced glutathione could ameliorate the function of mitochondria in the kidneys of STZ-induced diabetic rats to show nephroprotective effect.
