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[目的]观察氯胺酮对颅脑损伤大鼠血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及神经细胞凋亡的影响。[方法]实验共分3大组:伪手术组、损伤模型组、氯胺酮治疗组,后两组再根据取材时间分24h、72h、168h组。应用改良的Feeney自由落体法建立颅脑损伤模型,伪手术组只开骨窗,不打击致伤,治疗组造模方法与模型组相同,伤后1h腹腔注射氯胺酮120mg/kg,每隔12h加用1次,在规定时间取血清,检测TNF-α、IL-6含量;取损伤部位脑组织固定、包埋、切片,免疫组化法观察细胞凋亡。[结果]模型建立后,大鼠血清中TNF-α、IL-6含量明显升高,神经细胞凋亡明显增加,用氯胺酮治疗,能明显抑制血清中TNF-α、IL-6的升高和神经细胞凋亡的增加。[结论]氯胺酮能够抑制颅脑损伤大鼠血清TNF-α、IL-6的升高和凋亡细胞过表达,对颅脑损伤具有保护作用。
[Objective] To observe the effect of ketamine on serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and neuronal apoptosis in brain injury rats. [Methods] The experiment was divided into 3 groups: sham-operation group, injury model group and ketamine treatment group. The latter two groups were divided into two groups according to the time of 24 hours, 72 hours and 168 hours. The model of craniocerebral injury was established by modified Feeney free-fall method. The sham operation group only had open-ended windows and did not attack the wounds. The modeling method in the treatment group was the same as the model group. Ketamine 120 mg / kg Serum samples were taken at one time and TNF-α and IL-6 levels were measured. The brain tissue was fixed, embedded, sectioned and immunohistochemistry was used to observe the apoptosis. [Results] The levels of TNF-α and IL-6 in serum were significantly increased and the apoptosis of neurons was significantly increased after the model was established. Ketamine treatment significantly inhibited the increase of serum TNF-α and IL-6 Increased neuronal apoptosis. [Conclusion] Ketamine can inhibit the elevation of serum TNF-α and IL-6 levels and the over-expression of apoptotic cells in rats with brain injury and has a protective effect on brain injury.