大鼠创伤性脑损伤后诱导型NOS阳性表达与神经细胞凋亡的关系

Relation of induced nitric oxide synthase expression and apoptosis after traumatic brain injury in rats

目的 :探讨大鼠创伤性脑损伤 (TBI)后诱导型一氧化氮合酶 (i NOS)的表达和神经细胞凋亡的关系。方法 :将健康 SD大鼠随机分为假手术组、伤后 2 4 h组、伤后 72 h组、伤后 16 8h组。采用 i NOS免疫组化技术 ,研究大鼠创伤性脑损伤后 i NOS的表达变化及其细胞定位 ,采用凋亡细胞原位缺口末端标记法 (TUNEL ) ,观察大鼠在创伤性脑损伤后不同时点的神经细胞凋亡情况。结果 :大鼠创伤性脑损伤后 2 4 h大脑损伤区周围皮质和海马区 i NOS活性明显升高 ,伤后 72 hi NOS阳性表达最明显 ,伤后 16 8h仍有表达。大鼠创伤性脑损伤后 2 4 h大脑损伤区周围皮质和海马区神经细胞凋亡明显增多 ,伤后 72 h增多最明显 ,可持续 16 8h。结论 :TBI后损伤区周围皮质和伤侧海马的 i NOS阳性细胞呈高表达并与神经细胞的凋亡呈同步变化 ,推测 i NOS的表达可能参与了

Objective:To investigate the relation of the expression of induced nitric oxide synthase (iNOS) and cellular apoptosis after traumatic brain injury (TBI) in rats.Methods:Sprague-Dawley adult rats were used and randomly divided into four groups :shame group, 24h group, 72h group, 168h group. Immunohistochemistry,Nissl labeling and TdT mediated dUDP nick end labeling(TUNEL) were used to determine the expression of iNOS and apoptosis-associated signals in the hippocampus and cerebral cortex area after the injury. Results:TUNEL positive cells were identified as early as 24 hours post injury; and reached maximum level 72 hours later and then declined in ipsilateral hippocampus and the near-damaged-areas in the ipsilateral of the injuryed cortex. iNOS positive cells signficantly increased after 24 hours and reached a peak 72 hours post injury in the near-damaged-areas in the ipsilateral of the injuryed cortex and ipsilateral hippocampus.Conclusions:These evidences suggest that a temporal course of the expression of iNOS is initiated after TBI in selected brain region.The changes of TUNEL positive cells are consistent with iNOS positive cells .The express of iNOS may induce cell apoptosis.