右美托咪啶对创伤性脑损伤大鼠模型的神经保护作用实验研究

目的探讨右美托咪啶对创伤性脑损伤组织炎症与细胞凋亡影响。方法建立创伤性脑损伤大鼠模型,设置实验组和对照组,其中实验组予以右美托咪啶6μg/kg腹腔注射干预,对照组予以等量生理盐水腹腔注射,损伤后第3天和第7天,采用ELISA检测损伤组织内肿瘤坏死因子(TNF-α)和白介素-1β(IL-1β)浓度水平,Western-bolt分析损伤组织内凋亡信号关键蛋白caspase-3表达,TUNEL法观察损伤组织细胞凋亡情况。结果右美托咪啶处理可明显降低创伤性脑损伤组织内炎性因子TNF-α和IL-1β浓度(P0.05),减少凋亡信号关键蛋白caspase-3表达(P0.05),显著抑制创伤性脑损伤组织中神经细胞凋亡(P0.05)。结论右美托咪啶处理具有明显神经保护作用,其机制可能与减轻创伤性脑损伤组织炎性反应和抑制神经细胞凋亡有关。

Neuroprotective effect of dexmedetomidine in a rat model of traumatic brain injury:an experimental study

Objective To investigate the effect of dexmedetomidine on tissue inflammation and cell apoptosis in rats with traumatic brain injury (TBI).Methods A rat model of TBI was established.The rats were divided into experimental group and control group.The rats in the experimental group were given intraperitoneal injection of dexmedetomidine 6 μg/kg and those in the control group were given intraperitoneal injection of normal saline of the same volume.At 3 and 7 days after injury,ELISA was used to measure the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β),Western blot was used to measure the expression of caspase-3,and TUNEL was used to observe cell apoptosis.Results Dexmedetomidine treatment significantly reduced the concentrations of TNF-α and IL-1β (P ＜ 0.05) and the expression of caspase-3 (P ＜ 0.05) and inhibited the apoptosis of neural cells in traumatic brain tissue (P ＜ 0.05).Conclusions Dexmedetomidine exerts a marked neuroprotective effect by alleviating inflammatory response and inhibiting the apoptosis of neural cells in traumatic brain tissue.