南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2013年
10期
1489-1493
,共5页
何青春%刘婷%周利平%王爱民%李湘民
何青春%劉婷%週利平%王愛民%李湘民
하청춘%류정%주리평%왕애민%리상민
亚低温%心肺复苏%caspase-3%Bcl-2%Bax%凋亡
亞低溫%心肺複囌%caspase-3%Bcl-2%Bax%凋亡
아저온%심폐복소%caspase-3%Bcl-2%Bax%조망
mild hypothermia%cardiopulmonary resuscitation%apoptosis%caspase-3%Bcl-2%Bax
目的研究不同程度亚低温对大鼠心肺复苏(CPR)后脑组织凋亡的影响。方法利用窒息法制作心肺复苏模型,SD大鼠15只,随机分为对照组(正常体温)、34℃低温组、32℃低温组,每组各5只。对照组在CPR后置于室温25℃下常规治疗;34℃低温组(34+/-0.2℃)和32℃低温组(32+/-0.2℃)在CPR 0.5 h后分别给予亚低温治疗。各组大鼠均于CPR后12 h取脑组织,免疫组化法测定大脑皮层caspase-3蛋白表达,Western blotting测定Bcl-2、Bax表达,同时观察各组脑组织病理变化。结果与常温组相比,低温组神经元caspase-3表达均明显减弱(P<0.05),其中32℃低温组caspase-3表达减弱更加明显(P<0.05);低温组Bcl-2表达明显增强(P<0.05),32℃低温组的Bcl-2蛋白表达比34℃低温组表达更强;3组大鼠神经元凋亡蛋白bax的表达无明显差异。结论亚低温可能通过降低caspase-3蛋白的表达、增强Bcl-2的表达,从而抑制脑细胞凋亡减轻脑损伤,32℃亚低温治疗比34℃更能起到脑保护的作用。
目的研究不同程度亞低溫對大鼠心肺複囌(CPR)後腦組織凋亡的影響。方法利用窒息法製作心肺複囌模型,SD大鼠15隻,隨機分為對照組(正常體溫)、34℃低溫組、32℃低溫組,每組各5隻。對照組在CPR後置于室溫25℃下常規治療;34℃低溫組(34+/-0.2℃)和32℃低溫組(32+/-0.2℃)在CPR 0.5 h後分彆給予亞低溫治療。各組大鼠均于CPR後12 h取腦組織,免疫組化法測定大腦皮層caspase-3蛋白錶達,Western blotting測定Bcl-2、Bax錶達,同時觀察各組腦組織病理變化。結果與常溫組相比,低溫組神經元caspase-3錶達均明顯減弱(P<0.05),其中32℃低溫組caspase-3錶達減弱更加明顯(P<0.05);低溫組Bcl-2錶達明顯增彊(P<0.05),32℃低溫組的Bcl-2蛋白錶達比34℃低溫組錶達更彊;3組大鼠神經元凋亡蛋白bax的錶達無明顯差異。結論亞低溫可能通過降低caspase-3蛋白的錶達、增彊Bcl-2的錶達,從而抑製腦細胞凋亡減輕腦損傷,32℃亞低溫治療比34℃更能起到腦保護的作用。
목적연구불동정도아저온대대서심폐복소(CPR)후뇌조직조망적영향。방법이용질식법제작심폐복소모형,SD대서15지,수궤분위대조조(정상체온)、34℃저온조、32℃저온조,매조각5지。대조조재CPR후치우실온25℃하상규치료;34℃저온조(34+/-0.2℃)화32℃저온조(32+/-0.2℃)재CPR 0.5 h후분별급여아저온치료。각조대서균우CPR후12 h취뇌조직,면역조화법측정대뇌피층caspase-3단백표체,Western blotting측정Bcl-2、Bax표체,동시관찰각조뇌조직병리변화。결과여상온조상비,저온조신경원caspase-3표체균명현감약(P<0.05),기중32℃저온조caspase-3표체감약경가명현(P<0.05);저온조Bcl-2표체명현증강(P<0.05),32℃저온조적Bcl-2단백표체비34℃저온조표체경강;3조대서신경원조망단백bax적표체무명현차이。결론아저온가능통과강저caspase-3단백적표체、증강Bcl-2적표체,종이억제뇌세포조망감경뇌손상,32℃아저온치료비34℃경능기도뇌보호적작용。
Objective To explore the effect of mild to moderate hypothermia on the expressions of apoptosis-related genes in the brain tissue of rats after cardiopulmonary resuscitation (CPR). Methods CPR models were established by asphyxia in 15 male SD rats, which were randomized equally into normal temperature group, 34 ℃ hypothermia group and 32 ℃ hypothermia group. The brain tissues of the rats were obtained after treatment for 12 h to observe the pathological changes. The expression of caspase-3 in cerebral cortex neurons was determined with immunohistochemistry, and the expressions of Bcl-2 and Bax were detected by Western blotting. Results Compared with normal temperature group, the two hypothermia groups (especially 32℃group) showed significantly decreased expression of caspase-3 in the cortical neurons (P<0.05). Bcl-2 protein expression was significantly increased in the hypothermia groups, especially in 32℃hypothermia group (P<0.05). There was no significant difference in Bax protein expression among the 3 groups. Conclusion Mild hypothermia can relieve brain injury by down-regulating caspase-3 expression and up-regulating Bcl-2 protein expression to inhibit apoptosis of the brain neurons. Hypothermia at 32℃offers better protection of the brain tissue than hypothermia at 34℃.