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
2009年
3期
155-158
,共4页
王端玉%赵鑫%卜祥梅%王志刚
王耑玉%趙鑫%蔔祥梅%王誌剛
왕단옥%조흠%복상매%왕지강
热疗%凋亡%Bax%Bcl-2%Caspase-3
熱療%凋亡%Bax%Bcl-2%Caspase-3
열료%조망%Bax%Bcl-2%Caspase-3
Hyperthermia%Apoptosis%Bax%Bcl-2%Caspase-3
目的 观察用丙泊酚和水合氯醛全身麻醉建立全身高温模型的大鼠海马神经元凋亡蛋白的表达,探讨全身热疗诱导大鼠海马神经元凋亡的信号途径.方法 63只健康雄性Wister大鼠随机分为空白对照组(A组)、丙泊酚麻醉热疗组(B组)、水合氯醛麻醉热疗组(C组),每组21只.B、C两组热疗后24 h,A、B、C 3组大鼠同时断头取脑,采用TUNEL法检测海马神经元凋亡百分比,免疫组化法检测Bax、Bcl-2、caspase-3蛋白的表达,透射电镜观察神经元超微结构的变化.结果 B、C两组与A组比较,大鼠海马神经元超微结构发生改变,B组神经元超微结构损害较C组轻;B组和C组的海马神经元凋亡百分比和Bax、Bcl-2、caspase-3蛋白表达均高于A组(P<0.05),C组Bax、caspase-3阳性评分高于B组(P<0.05)、Bcl-2阳性评分低于B组(P<0.05).结论 全身热疗通过上调Bax、caspase-3表达和下调Bcl-2表达诱导大鼠海马神经元凋亡.
目的 觀察用丙泊酚和水閤氯醛全身痳醉建立全身高溫模型的大鼠海馬神經元凋亡蛋白的錶達,探討全身熱療誘導大鼠海馬神經元凋亡的信號途徑.方法 63隻健康雄性Wister大鼠隨機分為空白對照組(A組)、丙泊酚痳醉熱療組(B組)、水閤氯醛痳醉熱療組(C組),每組21隻.B、C兩組熱療後24 h,A、B、C 3組大鼠同時斷頭取腦,採用TUNEL法檢測海馬神經元凋亡百分比,免疫組化法檢測Bax、Bcl-2、caspase-3蛋白的錶達,透射電鏡觀察神經元超微結構的變化.結果 B、C兩組與A組比較,大鼠海馬神經元超微結構髮生改變,B組神經元超微結構損害較C組輕;B組和C組的海馬神經元凋亡百分比和Bax、Bcl-2、caspase-3蛋白錶達均高于A組(P<0.05),C組Bax、caspase-3暘性評分高于B組(P<0.05)、Bcl-2暘性評分低于B組(P<0.05).結論 全身熱療通過上調Bax、caspase-3錶達和下調Bcl-2錶達誘導大鼠海馬神經元凋亡.
목적 관찰용병박분화수합록철전신마취건립전신고온모형적대서해마신경원조망단백적표체,탐토전신열료유도대서해마신경원조망적신호도경.방법 63지건강웅성Wister대서수궤분위공백대조조(A조)、병박분마취열료조(B조)、수합록철마취열료조(C조),매조21지.B、C량조열료후24 h,A、B、C 3조대서동시단두취뇌,채용TUNEL법검측해마신경원조망백분비,면역조화법검측Bax、Bcl-2、caspase-3단백적표체,투사전경관찰신경원초미결구적변화.결과 B、C량조여A조비교,대서해마신경원초미결구발생개변,B조신경원초미결구손해교C조경;B조화C조적해마신경원조망백분비화Bax、Bcl-2、caspase-3단백표체균고우A조(P<0.05),C조Bax、caspase-3양성평분고우B조(P<0.05)、Bcl-2양성평분저우B조(P<0.05).결론 전신열료통과상조Bax、caspase-3표체화하조Bcl-2표체유도대서해마신경원조망.
Objective To observe the expression of neuron apoptotic protein caused by whole body gyperthermis (WBH) in rats anesthetized using propofol and chloral hydrate,and to explore the pathway of any hippocampal neuron apoptosis induced by WBH. Methods Sixty-three male Wistar rats were randomly divided into 3groups,21 in each group.One guoup received neither anesthesia nor WBH treatment sa a control (group A);group B were anesthetized with an intraperitoneal injection of 100 mg/kg of propofol;group C receivde a similar injection of chloral hydrate. This was followed by WBH (keeping the rats' core temperature at 42°for 30 min) for all three groups. The rats'brains were then removed 24 h after WBH to separate the ghpplcampal CA1,CA2 zones and the dentate gyrus regions.Any neuron apoptosis was detected using the TUNEL methol;Bax/Bcl-2/caspase-3 protein expression was measured with a SABC immmunogistochemical technique;and the changes in ultrastructure were observed tith an electron microscope. Results Compared with group A,the changes in the ultrastructure of neurons in the hippocampus changed after WBh were the most severe in group C.The changes included edema of the organelles,vacuolization of mitochondria,rarefaction of the endocytoplasmic reticulum,incopleasmic reticulum,incomplete synaptic membranes and autophagy.Both the number of apoptotic neurons and the expression of Bax and capase-3 protein in the hippocampus increased in the following order: group A<group B<group C.Expression of Bcl-2 protein in the hippocampus increased in the following order: group A<group C<group B. Conclusion Hippocampal apoptosis induced by WBh involves upregulating the expression of Bax and caspase-3 and downregulating the expression of Bcl-2.