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目的探讨NF-κB在颅脑损伤后继发氧化应激及细胞凋亡之间的关系及可能机制。方法成年健康雄性SD大鼠48只,随机分为对照组(n=6)和颅脑损伤组(n=42)。颅脑损伤组通过改良Feeney法建立颅脑损伤模型,根据伤后处死时间分为1、3、6、12及24小时、3和7天共7个亚组,每亚组各6只。每亚组随机取3只大鼠处死,取挫伤灶周围组织行脑组织超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)测定;剩余的3只大鼠采用免疫组织化学方法检测挫伤灶周围脑组织中NF-κB的表达情况,同时采用TUNEL法观察脑挫伤灶周围细胞凋亡情况。结果颅脑损伤后1小时可见NF-κB蛋白明显表达,3~12小时表达逐渐加强,并于24小时达到高峰,3~7天表达稍减弱,但仍为高表达状态;NF-κB蛋白表达与MDA、SOD及GSH相关(r=0.731,r=-0.702,r=-0.674,P值均<0.05),与细胞凋亡水平相关(r=0.720,P<0.05)。结论颅脑损伤后NF-κB蛋白表达的变化规律参与了继发性脑损伤中氧化应激反应及细胞凋亡等病理过程,抑制氧化应激水平,控制细胞凋亡,减少或减轻继发性脑损伤。
Objective To investigate the relationship between NF-κB and secondary oxidative stress and apoptosis after traumatic brain injury and its possible mechanism. Methods Forty-eight adult male Sprague Dawley rats were randomly divided into control group (n = 6) and craniocerebral injury group (n = 42). The traumatic brain injury model was established by the modified Feeney method. The injuries were divided into 1, 3, 6, 12 and 24 hours according to the time of injury. There were 7 subgroups in 3 and 7 days and 6 in each subgroup. Three rats in each subgroup were sacrificed at the same time. The contents of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) in brain tissue were determined. The remaining three rats Immunohistochemistry was used to detect the expression of NF-κB in the brain tissue around contusive contusion. TUNEL method was used to observe the apoptosis of cells around contusive contusion. Results One hour after craniocerebral injury, the expression of NF-κB protein was significantly increased. The expression of NF-κB protein gradually increased from 3 to 12 hours and peaked at 24 hours. The expression of NF-κB protein was still weakly elevated in 3-7 days. MDA, SOD and GSH (r = 0.731, r = -0.702, r = -0.674, all P <0.05), which were correlated with the level of apoptosis (r = 0.720, P <0.05). Conclusion The changes of NF-κB protein expression after traumatic brain injury are involved in the pathological process of oxidative stress and apoptosis in secondary brain injury, inhibiting the level of oxidative stress, controlling apoptosis, reducing or reducing the secondary Brain Injury.