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

发布时间：2018-08-15 17:23

【摘要】：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。
[Abstract]:Objective to investigate the effects of dexmetidine on inflammation and apoptosis in traumatic brain injury. Methods the model of traumatic brain injury was established in rats. The experimental group and the control group were treated with dexmetidine 6 渭 g/kg intraperitoneal injection, and the control group with the same amount of normal saline intraperitoneal injection on the 3rd and 7th day after injury. The levels of tumor necrosis factor (TNF- 伪) and interleukin-1 尾 (IL-1 尾) in injured tissue were detected by ELISA. Western-bolt was used to analyze the expression of caspase-3, a key protein of apoptosis signal in injured tissue. Tunel method was used to observe the apoptosis of injured tissue. Results dexmetidine significantly decreased the concentration of inflammatory factors TNF- 伪 and IL-1 尾 in traumatic brain injury (P0.05), decreased the expression of apoptosis signal key protein caspase-3 (P0.05), and significantly inhibited neuronal apoptosis in traumatic brain injury (P0.05). Conclusion dexmetidine has an obvious neuroprotective effect, and its mechanism may be related to the reduction of inflammatory response and inhibition of neuronal apoptosis in traumatic brain injury.
【作者单位】：齐齐哈尔医学院附属第一医院神经外科;齐齐哈尔医学院附属第一医院儿科;齐齐哈尔医学院附属第一医院康复科;
【基金】：基金项目:黑龙江省卫计委(2017-263)
【分类号】：R-332;R651.15

【相似文献】