| 朱 婧,张世平,李 鑫,赵义康,朱利娟.右旋氯胺酮对大鼠脊髓损伤后BDNF和炎症反应的影响[J].,2021,(19):3633-3637 |
| 右旋氯胺酮对大鼠脊髓损伤后BDNF和炎症反应的影响 |
| The Effect of Dextro-ketamine on BDNF and Inflammatory Response after Spinal Cord Injury in Rats |
| 投稿时间：2021-05-07 修订日期：2021-05-31 |
| DOI：10.13241/j.cnki.pmb.2021.19.007 |
| 中文关键词: 右旋氯胺酮 脊髓损伤 脑源性神经营养因子 原肌球蛋白受体激酶B 人肿瘤坏死因子-α 白介素1-β |
| 英文关键词: Dextral ketamine Spinal cord injury BDNF TrkB TNF-α IL-1β |
| 基金项目:陕西省自然科学基础研究计划项目（2018JM7121） |
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| 中文摘要: |
| 摘要 目的：探讨脊髓损伤后，使用右旋氯胺酮对BDNF和炎症因子TNF-α、IL-1β、IL-10、IL-13表达的影响。方法：将60只成年雄性大鼠随机分入5组，损伤组（A组）5 mg/kg右旋氯胺酮组（B组）、10 mg/kg右旋氯胺酮组（C组）和20 mg/kg右旋氯胺酮组（D组），假手术组（S组），每组12只。除S组外，其余4组使用脊髓打击法制备脊髓损伤模型，于脊髓损伤后4 h按照相应的给药剂量以5 mL/h的速度泵注右旋氯胺酮，S组仅进行手术操作，不损伤脊髓，手术后4h以相同的方法泵注等量的0.9 %氯化钠溶液。脊髓损伤后7、14、21和28天使用BBB法进行神经功能缺陷评分。采用HE染色法观察脊髓损伤后存活的神经元数量，ELISA法测定BDNF、Trk B、TNF-α、IL-1β、IL-10、IL-13、的表达水平。结果：与S组比较，其余四组BBB评分升高，存活神经元数量减少，BDNF、TrkB表达显著增加，促炎因子TNF-α、IL-1β表达上调，抑炎因子IL-10、IL-13表达均显著下调（P<0.05）；与A组比较，B组大鼠BBB评分、神经元数量、BDNF、TrkB、炎症因子的表达无明显差异（P>0.05），C组、D组大鼠BBB评分升高，存活神经元数量减少，BDNF、TrkB表达增多，促炎因子TNF-α、IL-1β上调，抑炎因子IL-10、IL-13表达下调，且差异有统计学意义(P<0.05)，C组与D组以上指标差异均无统计学意义（P>0.05）。结论：脊髓损伤后4 h给予10或20 mg/kg右旋氯胺酮可以减轻SCI后神经元损伤，其机制与上调原肌球蛋白受体激酶B（TrkB）的表达，增加BDNF含量，从而下调促炎因子IL-1β，TNF-α，上调抑炎因子 IL-10、IL-13有关，在本研究中右旋氯胺酮最佳作用剂量为10 mg/kg。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of dextral ketamine on the expression of BDNF and inflammatory cytokines TNF-α, IL-1β, IL-10 and IL-13 after spinal cord injury. Methods: 60 adult male rats were randomly divided into 5 groups: injury group (group A) 5 mg/kg dexamine group (group B), 10 mg/kg dexamine group (group C), 20 mg/kg dexamine group (group D) and sham operation group (group S), with 12 rats in each group. Except group S, spinal cord injury models were prepared by spinal cord shock method in the other 4 groups, and dextral ketamine was pumped at a rate of 5ml/h according to the corresponding dose 4h after spinal cord injury. Group S only underwent surgery without spinal cord injury, and the same amount of 0.9% sodium chloride solution was pumped 4 h after surgery in the same method. Neurological deficits were assessed using the BBB method at 7, 14, 21, and 28 days after spinal cord injury.The number of surviving neurons after spinal cord injury was observed by HE staining, and the expression levels of TNF-α, IL-1β, IL-10 and IL-13 were measured by ELISAS. Results: Compared with group S, BBB score was increased, the number of surviving neurons was decreased, the expression of BDNF was increased, the expressions of pro-inflammatory factors TNF-α and IL-1β were up-regulated, and the expressions of anti-inflammatory factors IL-10 and IL-13 were significantly down-regulated(P<0.05). Compared with group A, there were no significant differences in BBB score, number of neurons and expression of inflammatory cytokines in group B (P>0.05). The BBB score in group C and group D increased, the number of surviving neurons decreased, the expressions of pro-inflammatory cytokines TNF-α and IL-1β were up-regulated, and the expressions of anti-inflammatory cytokines IL-10 and IL-13 were significantly down-regulated(P<0.05). There was no statistically significant difference in the above indicators between group C and group D(P >0.05). Conclusion: Ketamine administration of 10 or 20 mg/kg 4h after spinal cord injury can alleviate SCI neuronal injury, and the mechanism may be related to the up-regulation of BDNF expression, down-regulation of pro-inflammatory factors TNF-α and IL-1β, and up-regulation of anti-inflammatory factors IL-10 and IL-13. In this study, the optimal dose of dextro-ketamine is 10 mg/kg. |
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