中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2015年
1期
46-50
,共5页
李晓峰%李吕力%肖继东%陈志%韦俊杰%韦旋%覃艳艳%封浑
李曉峰%李呂力%肖繼東%陳誌%韋俊傑%韋鏇%覃豔豔%封渾
리효봉%리려력%초계동%진지%위준걸%위선%담염염%봉혼
褪黑素%脑出血%小胶质细胞%氧化应激%超氧化物歧化酶%大鼠
褪黑素%腦齣血%小膠質細胞%氧化應激%超氧化物歧化酶%大鼠
퇴흑소%뇌출혈%소효질세포%양화응격%초양화물기화매%대서
Melatonin%Intracerebral hemorrhage%Microglia%Oxidative stress%Superoxide dismutase%Rats
目的 探讨褪黑素对大鼠脑出血后小胶质细胞激活与超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量变化的影响.方法 130只雄性SD大鼠,随机(随机数字法)分为正常组、假手术组、脑出血模型组(模型组)、褪黑素干预组(褪黑素组);组内随机分为12 h、1d、2d、4d、7d共5个时间点,按Rosenberg法建立脑出血模型,褪黑素组每天腹腔注射1 mg/mL褪黑素10 mL/kg;透射电镜技术观察脑出血后出血侧皮层小胶质细胞形态;免疫组织化学方法观察脑组织OX42阳性细胞动态表达;黄嘌呤氧化法和硫代巴比妥酸比色法检测脑组织SOD活性及MDA含量.结果 透射电镜显示,脑出血后2d时皮层神经元肿胀,小胶质细胞活化,褪黑素组小胶质细胞活化不明显;脑出血后12 h时血肿周围可见大量OX42阳性小胶质细胞表达,1d时达到高峰,7d时仍有表达,各时间点褪黑素组OX42阳性细胞表达明显低于模型组(P<0.05);脑出血后脑组织MDA含量(nmoL/mg prot)显著增加,7d时仍高于正常水平, (0.875 ±0.098) vs.(0.725±0.061),P<0.05; SOD活性(U/mg prot)变化则与之相反,(70.46 ±3.12) vs.(85.86 ±4.95),P <0.05.与模型组比较,褪黑素组MDA含量显著降低(P<0.05),SOD活性升高(P<0.05).结论 褪黑素对脑出血后神经细胞损伤具有保护作用,其机制可能与褪黑素减轻脑出血导致的氧化应激反应、抑制小胶质细胞活化相关.
目的 探討褪黑素對大鼠腦齣血後小膠質細胞激活與超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量變化的影響.方法 130隻雄性SD大鼠,隨機(隨機數字法)分為正常組、假手術組、腦齣血模型組(模型組)、褪黑素榦預組(褪黑素組);組內隨機分為12 h、1d、2d、4d、7d共5箇時間點,按Rosenberg法建立腦齣血模型,褪黑素組每天腹腔註射1 mg/mL褪黑素10 mL/kg;透射電鏡技術觀察腦齣血後齣血側皮層小膠質細胞形態;免疫組織化學方法觀察腦組織OX42暘性細胞動態錶達;黃嘌呤氧化法和硫代巴比妥痠比色法檢測腦組織SOD活性及MDA含量.結果 透射電鏡顯示,腦齣血後2d時皮層神經元腫脹,小膠質細胞活化,褪黑素組小膠質細胞活化不明顯;腦齣血後12 h時血腫週圍可見大量OX42暘性小膠質細胞錶達,1d時達到高峰,7d時仍有錶達,各時間點褪黑素組OX42暘性細胞錶達明顯低于模型組(P<0.05);腦齣血後腦組織MDA含量(nmoL/mg prot)顯著增加,7d時仍高于正常水平, (0.875 ±0.098) vs.(0.725±0.061),P<0.05; SOD活性(U/mg prot)變化則與之相反,(70.46 ±3.12) vs.(85.86 ±4.95),P <0.05.與模型組比較,褪黑素組MDA含量顯著降低(P<0.05),SOD活性升高(P<0.05).結論 褪黑素對腦齣血後神經細胞損傷具有保護作用,其機製可能與褪黑素減輕腦齣血導緻的氧化應激反應、抑製小膠質細胞活化相關.
목적 탐토퇴흑소대대서뇌출혈후소효질세포격활여초양화물기화매(SOD)활성、병이철(MDA)함량변화적영향.방법 130지웅성SD대서,수궤(수궤수자법)분위정상조、가수술조、뇌출혈모형조(모형조)、퇴흑소간예조(퇴흑소조);조내수궤분위12 h、1d、2d、4d、7d공5개시간점,안Rosenberg법건립뇌출혈모형,퇴흑소조매천복강주사1 mg/mL퇴흑소10 mL/kg;투사전경기술관찰뇌출혈후출혈측피층소효질세포형태;면역조직화학방법관찰뇌조직OX42양성세포동태표체;황표령양화법화류대파비타산비색법검측뇌조직SOD활성급MDA함량.결과 투사전경현시,뇌출혈후2d시피층신경원종창,소효질세포활화,퇴흑소조소효질세포활화불명현;뇌출혈후12 h시혈종주위가견대량OX42양성소효질세포표체,1d시체도고봉,7d시잉유표체,각시간점퇴흑소조OX42양성세포표체명현저우모형조(P<0.05);뇌출혈후뇌조직MDA함량(nmoL/mg prot)현저증가,7d시잉고우정상수평, (0.875 ±0.098) vs.(0.725±0.061),P<0.05; SOD활성(U/mg prot)변화칙여지상반,(70.46 ±3.12) vs.(85.86 ±4.95),P <0.05.여모형조비교,퇴흑소조MDA함량현저강저(P<0.05),SOD활성승고(P<0.05).결론 퇴흑소대뇌출혈후신경세포손상구유보호작용,기궤제가능여퇴흑소감경뇌출혈도치적양화응격반응、억제소효질세포활화상관.
Objective To investigate the effects of melatonin on activation of microglia and the changes of superoxide dismutase (SOD) and malondialdehyde (MDA) after intracerebral hemorrhage (ICH) in rats.Methods One hundred and thirty male SD rats were randomly divided into four groups:normal group,sham-operated group,intracerebral hemorrhage model group (Model group) and melatonin intervention group (MT group).Each group was further divided into 5 subgroups respectively at 12 h,1 d,2 d,4 d and 7 d after modeling.The ICH models were made in SD rats by using Rosenberg methods.Melatonin in dose of 10 mg/kg in solution of 1 mg/mL was given intraperitoneally to rats of MT group.The morphology of microglia was observed under electron microscope.OX42-positive cells were detected by immunohistochemical (ABC) methods.The contents of MDA or the activity of SOD was measured respectively by thiobarbituric acid or xanthine oxidation method.Results Electron microscope showed that the activation of microglia cell displayed in ameboid shape and swelling of neuron in hemisphere cortex in model group at 2 d after ICH,the activation of microglia cell of the cortex was insignificant in MT group.OX42-positive microglia cell in large amount surrounded the hematoma at 12 h after ICH,peaked at 1 d and lasted for 7 d.OX42-positive microglia cells in MT group were significantly fewer than that in model group at different intervals after ICH (P < 0.05).The content of MDA in model group increased signiflcantly after ICH,and higher than that in normal group at 7 d,[(0.875 ±0.098) nmol/mg prot vs.(0.725 ±0.061) nmol/mg prot,P <0.05,whereas the activity of SOD changes in the opposite direction,(70.46 ± 3.12) U/mg prot vs.(85.86 ± 4.95) /U/mg prot,P < 0.05.Compared with model group,the content of MDA were lower and the activity of SOD were higher in MT group after ICH (P < 0.05).Conclusion Melatonin provides a protective effect on the damage of nerve cell after ICH.The mechanism might be associated with melatonin by reducing the level of oxidative stress in brain tissue and attenuating the activation of microglia after ICH.