目的:探讨创伤性脑损伤(TBI)后神经型一氧化氮合酶羧基末端PDZ配体(CAPON)及其相关分子的表达变化及定位。方法:利用实时荧光定量PCR及蛋白免疫印迹技术研究大鼠脑损伤后CAPON及其相关分子Daxrasl、nNOS的mRNA及蛋白水平表达变化,利用免疫荧光双标技术检测脑损伤后CAPON分子的细胞定位情况。结果:大鼠TBI后1d-3d,CAPON分子mRNA和蛋白表达增加;Dexrasl及nNOS的表达变化趋势与CAPON的相一致。在损伤区CAPON主要表达于NeuN阳性的神经元;在损伤周边皮质中,CAPON与星型胶质细胞的标记物GFAP有少量共定位;此外,CAPON在OX-42阳性的小胶质细胞中也有少量的表达。结论:创伤性脑损伤后,CAPON及其相关分子(DaxrasI、nNOS)可被诱导表达,损伤神经细胞内的CAPON及其相关分子可能参与了TBI的病理进程。
Objective: To study the expression and localization of Carboxy-terminal PDZ ligand of neuronal nitric oxide synthase (CAPON) and its related molecules after rat traumatic brain injury (TBI). Methods: Realtime PCR analysis and Western blot assay were used to detect the mRNA and protein expression of CAPON and its related molecules (Dexrasl and nNOS) after rat TBI. Indirect immunofluorescence was employed to investigate the localization of CAPON. Results: The mRNA and protein expression of CAPON was increased on the lst~3rd day after TBI, and gradually recov- ered to the basal line level at lw. The expression patterns of Dexrasl and nNOS were similar to those of CAPON. Im- munofluorescence assay showed that CAPON was mainly expressed in neurons (NeuN-positive), some astrocytes (GFAP- positive) and a few microglia cells (OX42-positive) in the rat brain after TBI. Conclusion: The up-regulation of CAPON and its related molecules (Daxrasl and nNOS) may be involved in the pathogenic process of the traumatic brain injury.