CAJ | 학술논문

目的探讨不同程度的缺氧缺血(HI)对新生大鼠神经元凋亡和星形胶质细胞增生的影响.方法 72只日龄为7 d的Wistar大鼠随机平均分为假手术对照组、轻度HI组和重度HI组.后两组大鼠行右颈总动脉结扎,分剐置于含8%氧的密闭氧舱内34.5℃、40 min和35.5℃、65 min.用免疫组化法观察脑内胶质纤维酸性蛋白(GFAP)表达的变化;TUNEL染色评估细胞凋亡.结果与假手术对照组相比,轻度HI后48 h和1周缺血侧脑皮质与白质GFAP阳性细胞数均明显增加(P＜0.01,P＜0.05),有些区域GFAP阳性细胞增多可持续至4周(P＜0.05);重度HI后48 h和1周脑皮质与白质GFAP阳性细胞数明显多于假手术对照组(P＜0.01)和轻度HI组(P＜0.05),4周时GFAP阳性细胞不再增加.与假手术对照组相比,轻度HI后48 h、1周和4周,缺血侧皮质下白质TUNEL阳性细胞数量均明显增加(P＜0.05),而皮质阳性细胞数量无明显变化.重度HI后48 h缺血侧皮质与白质TUNEL阳性细胞数量均明显增加(P＜0.01),1周和4周梗死周边区TUNEL阳性细胞数量仍增加(P＜0.05).结论轻度缺氧缺血细胞凋亡主要局限于皮质下白质,星形胶质细胞增生持续较久;重度缺氧缺血可致缺血侧大脑半球广泛的细胞凋亡,星形胶质细胞增生短暂且强烈.
목적 탐토불동정도적결양결혈(HI)대신생대서신경원조망화성형효질세포증생적영향.방법 72지일령위7 d적Wistar대서수궤평균분위가수술대조조、경도HI조화중도HI조.후량조대서행우경총동맥결찰,분과치우함8%양적밀폐양창내34.5℃、40 min화35.5℃、65 min.용면역조화법관찰뇌내효질섬유산성단백(GFAP)표체적변화;TUNEL염색평고세포조망.결과 여가수술대조조상비,경도HI후48 h화1주결혈측뇌피질여백질GFAP양성세포수균명현증가(P＜0.01,P＜0.05),유사구역GFAP양성세포증다가지속지4주(P＜0.05);중도HI후48 h화1주뇌피질여백질GFAP양성세포수명현다우가수술대조조(P＜0.01)화경도HI조(P＜0.05),4주시GFAP양성세포불재증가.여가수술대조조상비,경도HI후48 h、1주화4주,결혈측피질하백질TUNEL양성세포수량균명현증가(P＜0.05),이피질양성세포수량무명현변화.중도HI후48 h결혈측피질여백질TUNEL양성세포수량균명현증가(P＜0.01),1주화4주경사주변구TUNEL양성세포수량잉증가(P＜0.05).결론 경도결양결혈세포조망주요국한우피질하백질,성형효질세포증생지속교구;중도결양결혈가치결혈측대뇌반구엄범적세포조망,성형효질세포증생단잠차강렬.
Objective To explore the effects of different degrees of hypoxia-ischemia(HI)on neuronal apoptosis and astrocyte proliferation in neonatal rats.Methods A total of 72 rat pups aged 7 days were randomly divided into 3 groups(n=24 each group):sham operated group,mild HI group,and severe HI group.The rats were subjected to right carotid artery occlusion and exposed to a hypoxic gas mixture (8% oxygen and 92% nitrogen)for 40 minutes at 34.5℃ in mild HI group and for 65 minutes at 35.5℃ in severe HI group.The expression of glial fibrillary acidic protein(GFAP)was detected by immunohistochemistry,and TUNEL method was performed to observe the proliferation of astrocytes and the neuronal apoptosis.Results Compared with sham operated group,the number of GFAP-positive cells signifiantly increased throughout the cortex and white matter in the ischemic hemisphere 48 hours(P＜0.01)and 1 week(P＜0.05)after mild HI,and in some areas the increase continued until week 4(P＜0.05).The number of GFAP-positive astrocytes in the cortex and white matter was signficantly higher in severe HI group than in mild HI group(P＜0.05)and sham operated group(P＜0.01)48 hours and 1 week after severe HI,but the increase was not detectable at week 4.Compared with sham operated group,the number of TUNEL-positive cells in the subcortical white matter in the ischemic hemisphere signficantly increased in mild HI group 48 hours,1 week,and 4 weeks following a mild HI insult(P＜0.05),but no signficant difference in the number of TUNEL-positive cells in the cortex was found.Following a severe HI insult,the number of TUNEL-positive cells in the cortex and white matter in the ischemic hemisphere significantly increased at 48 hours(P＜0.01),and in peri-infarct regions the number of TUNEL-positive cells increased until weeks 1 and 4(P＜0.05).Conclusion Mild HI causes neuronal apoptosis mainly in subcortical white matter and prolonged proliferation of astrocytes.Severe HI is associated with widespread neuronal apoptosis in the ischemic hemisphere,and the proliferation of astrocytes is rapid and prominent after severe HI.