中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2012年
1期
25-29
,共5页
刘江勤%陈超%郭佳林%姚明珠%陆国强
劉江勤%陳超%郭佳林%姚明珠%陸國彊
류강근%진초%곽가림%요명주%륙국강
婴儿持续高胰岛素血症性低血糖症%基质金属蛋白酶-2%谷胱甘肽%谷胱甘肽二硫化物%大鼠
嬰兒持續高胰島素血癥性低血糖癥%基質金屬蛋白酶-2%穀胱甘肽%穀胱甘肽二硫化物%大鼠
영인지속고이도소혈증성저혈당증%기질금속단백매-2%곡광감태%곡광감태이류화물%대서
Persistent hyperinsulinemia hypoglycemia of infancy%Matrix metalloproteinase-2%Glutathione%Glutathione disulfide%Rats
目的 研究7日龄新生大鼠持续低血糖对脑组织氧化应激和基质金属蛋白酶-2(matrix metalloproteinase-2,MMP-2)水平的影响,探讨低血糖引起新生儿脑损伤的机制. 方法 7日龄大鼠皮下注射普通胰岛素诱导持续性低血糖(n=6),观察36 h后收集脑皮质、海马和丘脑组织,采用谷胱甘肽活性测定试剂盒测定总谷胱甘肽( glutathione,GSH)和氧化型GSH( glutathione disulfide,GSSG)含量,计算GSSG/GSH,并采用酶谱法测定MMP-2活性.设正常血糖对照组6只.统计学方法采用t检验、双因素方差分析、单因素方差分析或Pearson相关性分析. 结果 持续低血糖36 h后,低血糖组脑组织总GSSG含量较对照组增高约1.5倍[(15.89±5.46)mg/g蛋白与(6.15±3.42) mg/g蛋白,t=3.704,P=0.004].GSSG/GSH比率也显著高于对照组[(5.58±1.79)％与(2.79±1.76)％,t=2.712,P=0.022)].低血糖组与对照组比较,大脑皮质和海马部位的GSSG/GSH比率差异无统计学意义,而丘脑GSSG含量和GSSG/GSH比率显著高于对照组[GSSG:(15.93±5.75)mg/g蛋白与(5.03±5.14)mg/g蛋白,P＜0.05; GSSG/GSH:(6.50±3.25)％与(2.41±3.12)％,P＜0.05].低血糖组脑组织MMP-2总活性较对照组显著增高(2.22±0.59与1.21±0.17,t=4.064,P=0.002).低血糖组与对照组脑组织不同部位比较,MMP-2活性均显著增高(皮质:2.14±0.51与1.17±0.27;海马:2.31±0.72与1.22±0.37;丘脑:2.22±0.68与1.24±0.18;三者P均＜0.0i).脑组织MMP-2活性与GSSG的含量和GSSG/GSH比率分别呈正相关(r=0.575和0.484,P=0.0002和0.0003). 结论 氧化应激是7日龄新生大鼠持续低血糖造成脑损伤的重要机制,其相关部位主要为丘脑.低血糖可使脑组织MMP-2活性升高,与GSSG和GSSG/GSH的含量有关.
目的 研究7日齡新生大鼠持續低血糖對腦組織氧化應激和基質金屬蛋白酶-2(matrix metalloproteinase-2,MMP-2)水平的影響,探討低血糖引起新生兒腦損傷的機製. 方法 7日齡大鼠皮下註射普通胰島素誘導持續性低血糖(n=6),觀察36 h後收集腦皮質、海馬和丘腦組織,採用穀胱甘肽活性測定試劑盒測定總穀胱甘肽( glutathione,GSH)和氧化型GSH( glutathione disulfide,GSSG)含量,計算GSSG/GSH,併採用酶譜法測定MMP-2活性.設正常血糖對照組6隻.統計學方法採用t檢驗、雙因素方差分析、單因素方差分析或Pearson相關性分析. 結果 持續低血糖36 h後,低血糖組腦組織總GSSG含量較對照組增高約1.5倍[(15.89±5.46)mg/g蛋白與(6.15±3.42) mg/g蛋白,t=3.704,P=0.004].GSSG/GSH比率也顯著高于對照組[(5.58±1.79)％與(2.79±1.76)％,t=2.712,P=0.022)].低血糖組與對照組比較,大腦皮質和海馬部位的GSSG/GSH比率差異無統計學意義,而丘腦GSSG含量和GSSG/GSH比率顯著高于對照組[GSSG:(15.93±5.75)mg/g蛋白與(5.03±5.14)mg/g蛋白,P＜0.05; GSSG/GSH:(6.50±3.25)％與(2.41±3.12)％,P＜0.05].低血糖組腦組織MMP-2總活性較對照組顯著增高(2.22±0.59與1.21±0.17,t=4.064,P=0.002).低血糖組與對照組腦組織不同部位比較,MMP-2活性均顯著增高(皮質:2.14±0.51與1.17±0.27;海馬:2.31±0.72與1.22±0.37;丘腦:2.22±0.68與1.24±0.18;三者P均＜0.0i).腦組織MMP-2活性與GSSG的含量和GSSG/GSH比率分彆呈正相關(r=0.575和0.484,P=0.0002和0.0003). 結論 氧化應激是7日齡新生大鼠持續低血糖造成腦損傷的重要機製,其相關部位主要為丘腦.低血糖可使腦組織MMP-2活性升高,與GSSG和GSSG/GSH的含量有關.
목적 연구7일령신생대서지속저혈당대뇌조직양화응격화기질금속단백매-2(matrix metalloproteinase-2,MMP-2)수평적영향,탐토저혈당인기신생인뇌손상적궤제. 방법 7일령대서피하주사보통이도소유도지속성저혈당(n=6),관찰36 h후수집뇌피질、해마화구뇌조직,채용곡광감태활성측정시제합측정총곡광감태( glutathione,GSH)화양화형GSH( glutathione disulfide,GSSG)함량,계산GSSG/GSH,병채용매보법측정MMP-2활성.설정상혈당대조조6지.통계학방법채용t검험、쌍인소방차분석、단인소방차분석혹Pearson상관성분석. 결과 지속저혈당36 h후,저혈당조뇌조직총GSSG함량교대조조증고약1.5배[(15.89±5.46)mg/g단백여(6.15±3.42) mg/g단백,t=3.704,P=0.004].GSSG/GSH비솔야현저고우대조조[(5.58±1.79)％여(2.79±1.76)％,t=2.712,P=0.022)].저혈당조여대조조비교,대뇌피질화해마부위적GSSG/GSH비솔차이무통계학의의,이구뇌GSSG함량화GSSG/GSH비솔현저고우대조조[GSSG:(15.93±5.75)mg/g단백여(5.03±5.14)mg/g단백,P＜0.05; GSSG/GSH:(6.50±3.25)％여(2.41±3.12)％,P＜0.05].저혈당조뇌조직MMP-2총활성교대조조현저증고(2.22±0.59여1.21±0.17,t=4.064,P=0.002).저혈당조여대조조뇌조직불동부위비교,MMP-2활성균현저증고(피질:2.14±0.51여1.17±0.27;해마:2.31±0.72여1.22±0.37;구뇌:2.22±0.68여1.24±0.18;삼자P균＜0.0i).뇌조직MMP-2활성여GSSG적함량화GSSG/GSH비솔분별정정상관(r=0.575화0.484,P=0.0002화0.0003). 결론 양화응격시7일령신생대서지속저혈당조성뇌손상적중요궤제,기상관부위주요위구뇌.저혈당가사뇌조직MMP-2활성승고,여GSSG화GSSG/GSH적함량유관.
Objective To investigate the effect of persistent hypoglycemia on the cerebral oxidative stress and matrix metalloproteinase-2 (MMP-2) activity of newborn rats and to explore the potential mechanism of hypoglycemia-induced brain injury of newborn. Methods Seven-day-old rats were injected insulin subcutaneously to induce persistent hypoglycemia.Cerebral cortex,hippocampus and thalamus were collected after 36 hours' observation and stored in -80 ℃.Glutathione (GSH)and glutathione disulfide (GSSG) were detected by commercial kit and GSSG/GSH was calculated.MMP-2 activity was detected by gelatin zymography. The data were analyzed by t test,one or two-wayanalysis of variance and Pearson correlation analysis.Six rats were set as the normal glucose group. Results Thirty-six hours after induction of hypoglycemia, the cerebral GSSG and GSSG/GSH of hypoglycemic pups elevated about 1.5 times higher than those of control group [GSSG:(15.89 ± 5.46) vs (6.15 ± 3.42) mg/g protein,t =3.704,P =0.004; GSSG/GSH:(5.58± 1.79) ％ vs (2.79±1.76) ％,t =2.712,P=0.022].The GSSG and GSSG/GSH in thalamus of hypoglycemia were significantly higher than those of control [GSSG:(15.93 ± 5.75) mg/g protein vs (5.03±5.14)mg/g protein,P＜0.05; GSSG/GSH:(6.50±3.25) ％ vs (2.41±3.12) ％,P＜0.05],whereas there were no significant differences in the cortex ard hippocampus.The total MMP-2 activity of hypoglycemic animals (2.22±0.59) was significantly higher than that of control (1.21± 0.17)(t=4.064,P=0.002),and significant differences were found between the two groups in cortex (2.14 ± 0.5 vs 1.17± 0.27),hippocampus (2.31± 0.72 vs 1.22 ± 0.37) and thalamus (2.22±0.68 vs 1.24±0.18) with all P＜0.01].The activity of MMP-2 was positively related to GSSG (r=0.575,P=0.0002) and GSSG/GSH (r=0.484,P=0.0003). Conclusions Oxidative stress might play an important role in the persistent hypoglycemia induced brain injury of 7-day-old rat pups and thalamus might be most vulnerable to hypoglycemia.Hypoglycemia might also elevate MMP-2 activity which is positively related to GSSG level and GSSG/GSH of the brain.
