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
2010年
11期
826-830
,共5页
全脑缺血再灌注%亚低温%星形胶质细胞%胶质纤维酸性蛋白%胀亡
全腦缺血再灌註%亞低溫%星形膠質細胞%膠質纖維痠性蛋白%脹亡
전뇌결혈재관주%아저온%성형효질세포%효질섬유산성단백%창망
Global cerebral ischemia and reperfusion%Mild hypothermia%Astrocytes%Glial fibrillary acidic protein%Oncosis
目的 研究大鼠全脑缺血再灌注后不同时间点海马CA1区星形胶质细胞胶质纤维酸性蛋白(GFAP)表达,观察超微结构变化,了解亚低温对其保护作用及影响.方法 制作大鼠全脑缺血模型,将96只大鼠分为常温组、亚低温组和假手术组,每组32只.根据缺血时间不同,每组再分为缺血6h、12h、24h、4d 4个亚组,每个亚组8只.苏木精-伊红(HE)染色观察海马CA1区细胞形态学改变,免疫组织化学方法检测胶质纤维酸性蛋白(GFAP)表达,原位氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL检测)及免疫组化双标染色观察海马CA1区星形胶质细胞的死亡方式,投射电镜观察星形胶质细胞超微结构改变,综合以上结果了解亚低温干预的效果.结果 大鼠全脑缺血再灌注后,GFAP表达随时间增加逐渐增强,亚低温组较常温组GFAP表达明显减少,4d时间点电镜下可见海马CA1区部分星形胶质细胞以胀亡形式死亡.结论 亚低温能明显减少GFAP的表达,对神经元有保护作用,全脑缺血再灌注后星形胶质细胞存在胀亡的死亡方式.
目的 研究大鼠全腦缺血再灌註後不同時間點海馬CA1區星形膠質細胞膠質纖維痠性蛋白(GFAP)錶達,觀察超微結構變化,瞭解亞低溫對其保護作用及影響.方法 製作大鼠全腦缺血模型,將96隻大鼠分為常溫組、亞低溫組和假手術組,每組32隻.根據缺血時間不同,每組再分為缺血6h、12h、24h、4d 4箇亞組,每箇亞組8隻.囌木精-伊紅(HE)染色觀察海馬CA1區細胞形態學改變,免疫組織化學方法檢測膠質纖維痠性蛋白(GFAP)錶達,原位氧覈苷痠轉移酶介導的dUTP缺口末耑標記(TUNEL檢測)及免疫組化雙標染色觀察海馬CA1區星形膠質細胞的死亡方式,投射電鏡觀察星形膠質細胞超微結構改變,綜閤以上結果瞭解亞低溫榦預的效果.結果 大鼠全腦缺血再灌註後,GFAP錶達隨時間增加逐漸增彊,亞低溫組較常溫組GFAP錶達明顯減少,4d時間點電鏡下可見海馬CA1區部分星形膠質細胞以脹亡形式死亡.結論 亞低溫能明顯減少GFAP的錶達,對神經元有保護作用,全腦缺血再灌註後星形膠質細胞存在脹亡的死亡方式.
목적 연구대서전뇌결혈재관주후불동시간점해마CA1구성형효질세포효질섬유산성단백(GFAP)표체,관찰초미결구변화,료해아저온대기보호작용급영향.방법 제작대서전뇌결혈모형,장96지대서분위상온조、아저온조화가수술조,매조32지.근거결혈시간불동,매조재분위결혈6h、12h、24h、4d 4개아조,매개아조8지.소목정-이홍(HE)염색관찰해마CA1구세포형태학개변,면역조직화학방법검측효질섬유산성단백(GFAP)표체,원위양핵감산전이매개도적dUTP결구말단표기(TUNEL검측)급면역조화쌍표염색관찰해마CA1구성형효질세포적사망방식,투사전경관찰성형효질세포초미결구개변,종합이상결과료해아저온간예적효과.결과 대서전뇌결혈재관주후,GFAP표체수시간증가축점증강,아저온조교상온조GFAP표체명현감소,4d시간점전경하가견해마CA1구부분성형효질세포이창망형식사망.결론 아저온능명현감소GFAP적표체,대신경원유보호작용,전뇌결혈재관주후성형효질세포존재창망적사망방식.
Objective To observe the expression of glial fibrillary acidic protein ( GFAP), and the pathological and ultrastructnral changes of astrocytes in the CA1 subfield of the hippocampus following global cerebral ischemia and reperfusion, and to explore the neuroprotective mechanism of mild hypothermia. Methods Global cerebral ischemia was established in rats by a modified version of Pulsinelli's method. Ninety-six rats were divided into three groups including a sham-operated group, a normothermic ischemic reperfusion (IR) group and a hypothermic ischemic reperfusion (HIR) group. Each group had four subgroups which were sacrificed for 6, 12 or 24 hours, or 4 days after reperfusion (for each subgroup n = 8 ). Hematoxylin-eosin (HE) staining was used to observe morphological changes in neurons in the CA1 subfield of the hippocampus. TUNEL methods were used to detect apoptosis among those neurons. Immunohistochemical staining was used to detect the expression of GFAP in the CA1 subfield and the mechanism of astrocyte pathology. GFAP TUNEL double-labeled immunohistochemistry was used with both the shamoperated and experimental groups. Electron microscopy was also used to evaluate morphological changes in astrocytes 24 hours and 4 days after ischemia and reperfusion. Results Compared with the sham-operated group, expression of GFAP immunoreactive positive cells increased gradually in the CA1 subfield of the IR group rats. Compared with the IR group, expression of GFAP immunoreactive positive cells was significantly lower in the HIR group at all time points. Microscopic observation at the 4th day showed that some astrocytes in the CA1 subfield had died through oncosis. Conclusions Mild hypothermia can significantly decrease the expression of GFAP immunoreactive positive cells and the number of apoptotic neurons in the CA1 subfield of the hippocampus, minimize cell oedema and provide protection for neurons. Oncosis kills astrocytes following global cerebral ischemia and reperfusion.
