中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2010年
12期
1025-1028
,共4页
吴晨光%王丽%高静%方春钱%徐志刚%柳迎昭%陈艳%陈宇宁
吳晨光%王麗%高靜%方春錢%徐誌剛%柳迎昭%陳豔%陳宇寧
오신광%왕려%고정%방춘전%서지강%류영소%진염%진우저
褪黑激素%糖尿病,实验性%线粒体%电压依赖性阴离子通道
褪黑激素%糖尿病,實驗性%線粒體%電壓依賴性陰離子通道
퇴흑격소%당뇨병,실험성%선립체%전압의뢰성음리자통도
Melatonin%Diabetes mellitus,experimental%Mitochondrial%Voltagedependent anion channel
目的 探讨褪黑素(melatonin,MT)对链脲佐菌素(streptozotocin,STZ)诱导的糖尿病大鼠线粒体功能的影响及其机制.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组和褪黑素干预组(褪黑素组),并以正常组作对照.干预8周后,观察各组大鼠心脏、肝脏及肾脏线粒体膜电位和肿胀度的变化,并通过免疫组化法分析线粒体外膜上的电压依赖性阴离子通道(voltage-dependent anion channel,VDAC)蛋白的表达.结果 (1)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏膜电位均明显升高,分别为[(553.6±193.5)mV对(311.4±133.7)mV,P＜0.05]、[(745.7±115.8)mV对(358.9±158.7)mV,P＜0.05]、[(951.6±246.1)mV对(425.8±177.9)mV,P＜0.05];(2)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏肿胀度趋势明显增强;(3)与糖尿病组比较,褪黑素组心脏、肝脏、肾脏VDAC表达均明显增加,分别为(76.93±8.263对58.59±7.62,P＜0.05)、(50.69±6.33对40.11±6.30,P＜0.05)、(77.86±8.59对61.44±12.86,P＜0.05).结论 褪黑素保护糖尿病大鼠心脏、肝脏及肾脏线粒体功能,初步推测可能与上调线粒体VDAC蛋白的表达有关.
目的 探討褪黑素(melatonin,MT)對鏈脲佐菌素(streptozotocin,STZ)誘導的糖尿病大鼠線粒體功能的影響及其機製.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組和褪黑素榦預組(褪黑素組),併以正常組作對照.榦預8週後,觀察各組大鼠心髒、肝髒及腎髒線粒體膜電位和腫脹度的變化,併通過免疫組化法分析線粒體外膜上的電壓依賴性陰離子通道(voltage-dependent anion channel,VDAC)蛋白的錶達.結果 (1)與糖尿病組比較,褪黑素組心髒、肝髒、腎髒膜電位均明顯升高,分彆為[(553.6±193.5)mV對(311.4±133.7)mV,P＜0.05]、[(745.7±115.8)mV對(358.9±158.7)mV,P＜0.05]、[(951.6±246.1)mV對(425.8±177.9)mV,P＜0.05];(2)與糖尿病組比較,褪黑素組心髒、肝髒、腎髒腫脹度趨勢明顯增彊;(3)與糖尿病組比較,褪黑素組心髒、肝髒、腎髒VDAC錶達均明顯增加,分彆為(76.93±8.263對58.59±7.62,P＜0.05)、(50.69±6.33對40.11±6.30,P＜0.05)、(77.86±8.59對61.44±12.86,P＜0.05).結論 褪黑素保護糖尿病大鼠心髒、肝髒及腎髒線粒體功能,初步推測可能與上調線粒體VDAC蛋白的錶達有關.
목적 탐토퇴흑소(melatonin,MT)대련뇨좌균소(streptozotocin,STZ)유도적당뇨병대서선립체공능적영향급기궤제.방법 STZ유도당뇨병대서모형,장당뇨병대서수궤분위당뇨병조화퇴흑소간예조(퇴흑소조),병이정상조작대조.간예8주후,관찰각조대서심장、간장급신장선립체막전위화종창도적변화,병통과면역조화법분석선립체외막상적전압의뢰성음리자통도(voltage-dependent anion channel,VDAC)단백적표체.결과 (1)여당뇨병조비교,퇴흑소조심장、간장、신장막전위균명현승고,분별위[(553.6±193.5)mV대(311.4±133.7)mV,P＜0.05]、[(745.7±115.8)mV대(358.9±158.7)mV,P＜0.05]、[(951.6±246.1)mV대(425.8±177.9)mV,P＜0.05];(2)여당뇨병조비교,퇴흑소조심장、간장、신장종창도추세명현증강;(3)여당뇨병조비교,퇴흑소조심장、간장、신장VDAC표체균명현증가,분별위(76.93±8.263대58.59±7.62,P＜0.05)、(50.69±6.33대40.11±6.30,P＜0.05)、(77.86±8.59대61.44±12.86,P＜0.05).결론 퇴흑소보호당뇨병대서심장、간장급신장선립체공능,초보추측가능여상조선립체VDAC단백적표체유관.
Objective To explore the effect of melatonin on mitochondria in streptozotocin (STZ)-induced diabetic rats and its potential mechanism. Methods The diabetic rat models were induced by intraperitoneal injection of STZ, and the diabetic rats were randomly divided into two groups: diabetes mellitus group (DM group) and melatonin-treated group (DM± MT group). The normal non-diabetic rats were served as control group. Mitochondrial membrane potential and mitochondrial swelling were measured, the expression of voltage-dependent anion channel (VDAC)was assayed by immunohistochemistry in the heart, liver and kidney among the different groups after 8 weeks. Results (1)Compared with DM group, mitochondrial membrane potential in the heart,liver and kidney were significantly elevated in DM± MT group (553.6± 193.5 vs. 311.4 ± 133.7;745.7±115.8 vs. 358.9±158.7; 951.6±246.1 vs. 425.8±177.9, all P＜0.05). (2)Compared with DM group, mitochondrial swelling in the heart, liver and kidney was reinforced in DM ± MT group. (3)Compared with DM group, the expressions of VDAC in the heart, liver and kidney were significantly up-regulated in DM± MT group (76.93 ± 8.263 vs. 58.59 ± 7.62, 50.69 ± 6.33 vs.40.11±6.30, 77.86±8.59 vs. 61.44± 12.86, all P＜0.05). Conclusions Melatonin has protective effect on the activity of mitochondria in the heart, liver and kidney in diabetic rats possibly by up-regulating the expression of VDAC.
