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目的研究FTY720对颅脑损伤大鼠认知功能的影响及相关机制。方法选用健康Wistar大鼠60只,♂,随机分成假手术组、模型组和治疗组,每组20只,采用改进的Feeney自由落体损伤装置建立大鼠颅脑损伤模型,分别于模型形成前给予-1 m L 0.9%氯化钠注射液或1 mg·kg1 FTY720腹腔注射。各组取10只大鼠,采用Morris水迷宫定位航行实验,记录大鼠逃避潜伏期,评价认知功能。另外各组取10只大鼠断头处死,分离海马组织,采用HE染色观察神经细胞形态,采用ELISA法检测脑组织白介素-1β、肿瘤坏死因子-α和白介素-6浓度。结果模型组大鼠逃避潜伏期较假手术组显著延长(P<0.05),海马组织神经细胞结构较假手术组明显破坏(P<0.05),脑组织白介素-1β、肿瘤坏死因子-α和白介素-6浓度较假手术组显著升高(P<0.05)。治疗组大鼠逃避潜伏期较模型组显著缩短(P<0.05),海马组织神经细胞结构较模型组明显恢复(P<0.05),脑组织白介素-1β、肿瘤坏死因子-α和白介素-6浓度较模型组显著下降(P<0.05)。结论 FTY720可显著改善颅脑损伤大鼠认知功能,其作用机制可能与FTY720的中枢炎症抑制作用有关。
Objective To investigate the effect of FTY720 on cognitive function in rats with brain injury and its related mechanisms. Methods Sixty healthy Wistar rats were randomly divided into sham operation group, model group and treatment group, with 20 rats in each group. The traumatic brain injury models were established by the modified Feeney free-fall injury device and were given before model formation -1 m L 0.9% sodium chloride injection or 1 mg · kg -1 FTY720 intraperitoneal injection. In each group, 10 rats were taken and Morris water maze positioning navigation experiment was used to record the escape latency and evaluate the cognitive function. In addition, 10 rats in each group were sacrificed and the hippocampus was separated. The morphology of neurons was observed by HE staining. The concentrations of interleukin-1β, tumor necrosis factor-α and interleukin-6 were detected by ELISA. Results The escape latency in model group was significantly longer than that in sham operation group (P <0.05). The structure of hippocampal neurons was significantly damaged than that in sham operation group (P <0.05). The levels of interleukin - 1β, tumor necrosis factor - α and interleukin - 6 concentration was significantly higher than the sham operation group (P <0.05). Compared with the model group, the escape latency of the treatment group was significantly shorter than that of the model group (P <0.05). The structure of hippocampal neurons recovered significantly compared with the model group (P <0.05). The concentrations of interleukin-1β, tumor necrosis factor-α and interleukin- The model group decreased significantly (P <0.05). Conclusion FTY720 can significantly improve the cognitive function in rats with traumatic brain injury and its mechanism may be related to the inhibition of central inflammation by FTY720.