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目的:观察单羧酸转运体-1(monocarboxylate transporter-1,MCT1)在不同发育时期及缺血缺氧(hypoxia-ischemia,HI)损伤模型大鼠胼胝体内的表达。方法:采用多聚甲醛灌注固定7 d、14 d、21 d和28 d SD大鼠脑组织,冰冻切片后进行MCT1/CNPase和MCT1/GFAP免疫荧光双标,观察胼胝体内MCT1在少突胶质细胞和星形胶质细胞的表达;另选生后3 d的SD大鼠,右侧颈总动脉结扎及缺氧处理以建立HI性脑白质损伤模型,至生后28d观察胼胝体MCT1的表达。结果:MCT1分别与CNPase和GFAP免疫荧光双标显示,生后早期,正常大鼠胼胝体内MCT1主要在GFAP阳性细胞表达,随生长时间延长,MCT1在CNPase阳性细胞的表达增加,而在GFAP阳性细胞的表达逐渐减少;HI损伤后28 d,MCT1/GAFP免疫荧光强度较对照组显著升高(P<0.01),而MCT1/CNPase的表达较对照组显著降低(P<0.01)。结论:在成年SD大鼠胼胝体,MCT1主要在CNPase阳性的少突胶质细胞表达,而HI脑白质损伤后,MCT1主要在星形胶质细胞表达。
OBJECTIVE: To observe the expression of monocarboxylate transporter-1 (MCT1) in corpus callosum of different developmental stages and hypoxia-ischemia (HI) model rats. Methods: The brains of SD rats were fixed with paraformaldehyde for 7 days, 14 days, 21 days and 28 days. After frozen section, MCT1 / CNPase and MCT1 / GFAP double immunofluorescence double labeling were used to detect the expression of MCT1 in oligodendrocytes The expression of MCT1 in the corpus callosum was observed at 28 days after birth in SD rats of 3 days after birth and ligation of the right common carotid artery and hypoxia to establish HI model of white matter injury. Results: MCT1 double immunofluorescence with CNPase and GFAP, respectively, showed that MCT1 was mainly expressed in GFAP positive cells in normal corpus callosum. The expression of MCT1 in CNPase positive cells increased with the prolongation of growth time, while in GFAP positive cells (P <0.01), while the expression of MCT1 / CNPase was significantly lower than that of the control group (P <0.01). CONCLUSION: MCT1 is mainly expressed in CNPase-positive oligodendrocytes in adult Sprague-Dawley rats, while MCT1 is mainly expressed in astrocytes after HI white matter injury.