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目的:通过观察肿瘤坏死因子(TNF-α)以及核转录因子κB(NF-κB)在颅脑损伤后脑组织中的表达变化,初步探讨两者在颅脑损伤后继发性脑损伤中的意义。方法:健康成年雄性SD大鼠64只,体重230-310g,随机分成对照组8只和颅脑损伤组56只,颅脑损伤组在外伤后1h、3h、6h、12h、24h、3d、7d处死,每组处死8只。取损伤灶周围的脑组织进行含水量以及超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)的测定,并进行病理切片观察其病理变化,最后用免疫组化法检测脑组织中TNF-α和NF-κB的含量。结果:1成功构建大鼠颅脑损伤的模型,颅脑损伤后的各时间点神经功能评分差异无统计学意义(P>0.05);2颅脑损伤组大鼠的脑组织含水量较对照组显著升高,并且在3d达到高峰,7d时逐渐下降,但仍高于对照组,差异有统计学意义(P<0.05);3大鼠颅脑损伤后切片表现为有大量的炎症细胞积聚,并有不同程度的脑细胞水肿,随着时间的推移逐渐加重,在第7d时,水肿较之前减轻,但仍有大量的炎性细胞浸润以及少量的纤维组织增生;4大鼠颅脑损伤后1h开始,损伤灶周围的脑组织中MDA的含量显著升高,且在之后的时间内持续升高,在3d时达到高峰,随后下降,7d时表达仍然高于对照组,而损伤组的SOD活性及GSH的活力明显降低,在7d时仍低于对照组,差异有统计学意义(P<0.05);5TNF-α以及NF-κB在颅脑损伤组中含量显著高于对照组,且在颅脑损伤后1h开始升高,在3d左右达到高峰,7d时稍有降低,但仍高于对照组,为高表达状态。结论:颅脑损伤后TNF-α以及NF-κB的变化趋势与继发性脑损伤的临床表现一致,参与了继发性脑损伤的病理过程。
OBJECTIVE: To investigate the changes of tumor necrosis factor (TNF-α) and nuclear factor-κB (NF-κB) in brain tissue after craniocerebral injury and to explore their significance in secondary brain injury following craniocerebral injury. Methods: Sixty-four healthy adult male Sprague-Dawley rats weighing 230-310 g were randomly divided into control group (n = 8) and craniocerebral injury group (n = 56). The traumatic brain injury group was treated at 1h, 3h, 6h, 12h, 24h, 3d, Executed, each executed 8. The water content, the content of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) in the brain tissue around the lesion were measured. The pathological changes were observed by pathological sections. The levels of TNF-α and NF-κB in brain tissue were detected by immunohistochemistry. Results: 1 The model of traumatic brain injury in rats was successfully established. There was no significant difference in the scores of neurological function at each time point after traumatic brain injury (P> 0.05). The brain water content of rats in traumatic brain injury group was significantly higher than that in control group (P <0.05). The sections of 3 rats after traumatic brain injury showed a large number of inflammatory cells accumulating, which were significantly higher than those of the control group (P <0.05) And had different degrees of brain cell edema, with the gradual increase over time, in the first 7d, edema than before, but there are still a large number of inflammatory cell infiltration and a small amount of fibrous tissue proliferation; 4 rats after traumatic brain injury 1h, MDA content in the brain tissue around the lesion increased significantly, and continued to rise in the later time, peaked at 3d, then decreased and remained higher than the control group on the 7th day, while SOD (P <0.05). The content of 5TNF-α and NF-κB in the brain injury group was significantly higher than that in the control group, and the difference was statistically significant The brain injury began to rise at 1h, peaked at about 3d, slightly decreased at 7d, but still higher than that at According to the group, for the high expression state. CONCLUSION: The changes of TNF-α and NF-κB in traumatic brain injury are consistent with the clinical manifestations of secondary brain injury and are involved in the pathological process of secondary brain injury.