中华物理医学与康复杂志
中華物理醫學與康複雜誌
중화물리의학여강복잡지
CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
2014年
2期
86-90
,共5页
脑缺血再灌注%亚低温%内皮-单核细胞激活多肽Ⅱ%大鼠
腦缺血再灌註%亞低溫%內皮-單覈細胞激活多肽Ⅱ%大鼠
뇌결혈재관주%아저온%내피-단핵세포격활다태Ⅱ%대서
Cerebral ischemia%Cerebral reperfusion%Hypothermia%EMAP-Ⅱ%Apoptosis
目的 通过观察局部亚低温干预对大鼠脑缺血再灌注后缺血半暗带区内皮-单核细胞激活多肽Ⅱ(EMAPⅡ)、EMAPⅡ前蛋白(proEMAPⅡ)表达的影响,从而探讨局部亚低温干预的脑保护机制.方法 共选取雄性Wistar大鼠44只,采用随机数字表法将其分为假手术组、常温组及亚低温组.采用改良Longa线栓法将常温组及亚低温组大鼠制成大脑中动脉缺血再灌注模型,亚低温组于再灌注后立即给予亚低温干预(持续治疗6h).于脑缺血再灌注后6h、12h、24 h、48 h及72 h时处死大鼠并取脑,采用HE染色观察各组大鼠神经细胞受损情况,采用免疫组化染色法比较各组大鼠缺血脑组织EMAPⅡ、proEMAPⅡ阳性细胞表达情况.结果 常温组及亚低温组EMAPⅡ阳性细胞均于缺血再灌注6h时明显表达,于再灌注24 h时达到峰值,随后逐渐下降；2组大鼠proEMAPⅡ阳性细胞均于缺血再灌注6h时明显表达,之后亚低温组逐渐下降,常温组于再灌注12h达到峰值后开始下降,至再灌注72 h时2组大鼠proEMAPⅡ阳性表达均已接近假手术组水平.亚低温组EMAPⅡ阳性表达在脑缺血再灌注6h、12h、24 h、48 h及72 h时均较常温组显著减少(P＜0.05).常温组proEMAPⅡ阳性细胞数量在脑缺血再灌注6h、12h及24 h时均较亚低温组明显增多.结论 局部亚低温干预能减弱大鼠缺血半暗带区EMAPⅡ、proEMAPⅡ阳性表达,抑制缺血再灌注损伤导致的细胞凋亡及炎性反应,从而发挥神经保护作用.
目的 通過觀察跼部亞低溫榦預對大鼠腦缺血再灌註後缺血半暗帶區內皮-單覈細胞激活多肽Ⅱ(EMAPⅡ)、EMAPⅡ前蛋白(proEMAPⅡ)錶達的影響,從而探討跼部亞低溫榦預的腦保護機製.方法 共選取雄性Wistar大鼠44隻,採用隨機數字錶法將其分為假手術組、常溫組及亞低溫組.採用改良Longa線栓法將常溫組及亞低溫組大鼠製成大腦中動脈缺血再灌註模型,亞低溫組于再灌註後立即給予亞低溫榦預(持續治療6h).于腦缺血再灌註後6h、12h、24 h、48 h及72 h時處死大鼠併取腦,採用HE染色觀察各組大鼠神經細胞受損情況,採用免疫組化染色法比較各組大鼠缺血腦組織EMAPⅡ、proEMAPⅡ暘性細胞錶達情況.結果 常溫組及亞低溫組EMAPⅡ暘性細胞均于缺血再灌註6h時明顯錶達,于再灌註24 h時達到峰值,隨後逐漸下降；2組大鼠proEMAPⅡ暘性細胞均于缺血再灌註6h時明顯錶達,之後亞低溫組逐漸下降,常溫組于再灌註12h達到峰值後開始下降,至再灌註72 h時2組大鼠proEMAPⅡ暘性錶達均已接近假手術組水平.亞低溫組EMAPⅡ暘性錶達在腦缺血再灌註6h、12h、24 h、48 h及72 h時均較常溫組顯著減少(P＜0.05).常溫組proEMAPⅡ暘性細胞數量在腦缺血再灌註6h、12h及24 h時均較亞低溫組明顯增多.結論 跼部亞低溫榦預能減弱大鼠缺血半暗帶區EMAPⅡ、proEMAPⅡ暘性錶達,抑製缺血再灌註損傷導緻的細胞凋亡及炎性反應,從而髮揮神經保護作用.
목적 통과관찰국부아저온간예대대서뇌결혈재관주후결혈반암대구내피-단핵세포격활다태Ⅱ(EMAPⅡ)、EMAPⅡ전단백(proEMAPⅡ)표체적영향,종이탐토국부아저온간예적뇌보호궤제.방법 공선취웅성Wistar대서44지,채용수궤수자표법장기분위가수술조、상온조급아저온조.채용개량Longa선전법장상온조급아저온조대서제성대뇌중동맥결혈재관주모형,아저온조우재관주후립즉급여아저온간예(지속치료6h).우뇌결혈재관주후6h、12h、24 h、48 h급72 h시처사대서병취뇌,채용HE염색관찰각조대서신경세포수손정황,채용면역조화염색법비교각조대서결혈뇌조직EMAPⅡ、proEMAPⅡ양성세포표체정황.결과 상온조급아저온조EMAPⅡ양성세포균우결혈재관주6h시명현표체,우재관주24 h시체도봉치,수후축점하강；2조대서proEMAPⅡ양성세포균우결혈재관주6h시명현표체,지후아저온조축점하강,상온조우재관주12h체도봉치후개시하강,지재관주72 h시2조대서proEMAPⅡ양성표체균이접근가수술조수평.아저온조EMAPⅡ양성표체재뇌결혈재관주6h、12h、24 h、48 h급72 h시균교상온조현저감소(P＜0.05).상온조proEMAPⅡ양성세포수량재뇌결혈재관주6h、12h급24 h시균교아저온조명현증다.결론 국부아저온간예능감약대서결혈반암대구EMAPⅡ、proEMAPⅡ양성표체,억제결혈재관주손상도치적세포조망급염성반응,종이발휘신경보호작용.
Objective To investigate the effects of local mild hypothermia on the expression of EMAP-Ⅱ and proEMAP-Ⅱ after cerebral ischemia and reperfusion in rats and to explore the possible neuroprotection mechanism of mild hypothermia.Methods Forty-four male Wistar rats were divided randomly into a sham-operation group (Sham),a normothermia group (NT) and a hypothermia group (HT).Middle cerebral artery occlusion was performed using Longa's method,and reperfusion was allowed after 2 hours of occlusion.Mild hypothermia (33.0 ± 0.5)℃ for 6 hours was initiated at the start of reperfusion,followed by rewarming.Brains were harvested after 6,12,24,48 and 72 hours of reperfusion and used for HE staining to evaluate cellular apzoptosis and immunohistochemical staining for detecting the expression EMAP-Ⅱ and proEMAP-Ⅱ.Results The expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbra was significant at 6 hours in the normothermia and hypothermia groups.It peaked at 12 hours in the normothermia group and 24 hours in the hypothermia group,and then decreased gradually.At 72 hours the expression of EMAP-Ⅱ and proEMAP-Ⅱ in the ischemic penumbras was very close to that in the sham group.EMAP-Ⅱ-positive cells were significantly fewer in the hypothermia group than in the normothermia group at all time points.ProEMAP-Ⅱ-positive cells were significantly more numerous in the normothermia group than in the hypothermia group at 6,12 and 24 hours.Conclusions Mild hypothermia (33.0 ± 0.5) ℃ has a valid neuroprotective effect which involves reducing EMAP-Ⅱ and proEMAP-Ⅱ expression in the ischemic penumbra and inhibiting apoptosis and inflammatory reactions after cerebral ischemia and reperfusion,at least in rats.
