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基于p38MAPK信号通路分析咪达唑仑对腰椎间盘突出症模型大鼠疼痛的影响
Hits: 1772   Download times: 599   Received:March 11, 2022    
作者Author单位UnitE-Mail
刘建 LIU Jian 开滦总医院赵各庄医院麻醉科, 河北 古治 063101 Department of Anesthesiology, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China  
叶玉军 YE Yu-jun 唐山市中医医院麻醉科, 河北 唐山 063000 Department of Anesthesiology, Tangshan Hospital of Traditional Chinese Medicine, Tangshan 063000, Hebei, China xxhq3n@163.com 
刘树民 LIU Shu-min 开滦总医院赵各庄医院麻醉科, 河北 古治 063101 Department of Anesthesiology, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China  
刘爽 LIU Shuang 开滦总医院赵各庄医院外科, 河北 古治 063101 Department of Surgery, Kailuan General Hospital Zhaogezhuang Hospital, Guzhi 063101, Hebei, China  
期刊信息:《中国骨伤》2023年36卷,第1期,第55-60页
DOI:10.12200/j.issn.1003-0034.2023.01.010
基金项目:河北省医学科学研究计划(编号:20201290)


目的:探究基于p38MAPK信号通路分析咪达唑仑对腰椎间盘突出症模型大鼠疼痛的影响。

方法:选取50只SPF级别SD健康大鼠,雌雄各半,随机分为正常组,模型组,低、中、高剂量组,模型组和低、中、高剂量组先建立腰椎间盘突出症模型。正常组、模型组大鼠腹腔注射生理盐水,低、中、高剂量组大鼠腹腔注射咪达唑仑,分别按30、60、90 mg/kg给药。采用酶联免疫吸检测大鼠血清中白细胞介素-1β(interleukin-1β,IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、5-羟色胺(5-hydroxytryptamine,5-HT)、β-内啡肽(β-endorphin,β-EP)、P物质(substance P,SP)、神经肽Y(neuropeptide Y,NPY)水平,采用Western blot检测各组大鼠组织中p38 MAPK,基质金属蛋白酶3(matrix metalloproteinase-3,MMP3)蛋白表达。

结果:模型组大鼠TNF-α、IL-1β、β-EP水平较正常组高,5-HT水平低于正常组(P<0.05);低、中、高剂量组大鼠TNF-α、IL-1β、β-EP水平较模型组下降、5-HT水平升高(P<0.05)。模型组大鼠较正常组SP、NPY水平上升(P<0.05);低、中、高剂量组较模型组大鼠SP、NPY水平下降(P<0.05)。模型组较正常组大鼠p38 MAPK、MMP-3表达上升(P<0.05),低、中、高剂量较模型组大鼠p38 MAPK、MMP-3表达下降(P<0.05)。

结论:咪达唑仑可以改善腰椎间盘突出症模型大鼠的免疫炎症反应,可能是通过p38MAPK信号通路调控来实现的。
[关键词]:p38MAPK信号通路  椎间盘移位  免疫  炎症  腰椎  疼痛
 
Analysis of the effect of midazolam on pain in a rat model of lumbar disc herniation based on the p38 MAPK signaling pathway
Abstract:

Objective To investigate the effect of midazolam on pain in lumbar disc herniation model rats based on p38 MAPK signaling pathway.

Methods Fifty SPF-grade Sprague-Dawley healthy rats,half male and half female,were selected and randomly divided into normal group,model group,and low-dose,medium-dose,high-dose groups. Model group and low-dose,medium-dose,high-dose groups were initially modeled for lumbar disc herniation. Intraperitoneal injection of saline was performed in rats of normal and model groups; and in the low-dose,medium-dose,and high-dose groups,intraperitoneal injection of midazolam was performed with doses of 30,60,and 90 mg/kg,respectively. Interleukin-1β (IL-1β),tumor necrosis factor-α (TNF-α),5-hydroxytryptamine (5-HT),β-endorphin (β-EP),substance P (SP),neuropeptide Y (NPY) were detected in the serum of rats by enzyme-linked immunoassay. The expression of p38 MAPK and matrix metalloproteinase-3(MMP-3) protein were detected by Western blot in the tissues of rats of each group.

Results The levels of TNF-α,IL-1β and β-EP were higher and the level of 5-HT was lower in the model group than in the normal group(P<0.05);the levels of TNF-α,IL-1β and β-EP were lower and the level of 5-HT was higher in the low-dose,medium-dose and high-dose groups than in the model group(P<0.05). The levels of SP and NPY increased in the model group compared with the normal group (P<0.05) and the levels of SP and NPY decreased in the low-dose,medium-dose and high-dose groups compared with the model group (P<0.05). The expression of p38 MAPK and MMP-3 increased in the model group compared with the normal group (P<0.05); the expression of p38 MAPK and MMP-3 decreased in the low-dose,medium-dose and high-dose compared with the model group(P<0.05).

Conclusion Midazolam may ameliorate the immune inflammatory response in rats with a model of lumbar disc herniation,possibly regulated through the p38MAPK signaling pathway.
KEYWORDS:p38MAPK signaling pathway  Intervertebral disk displacement  Immunity  Inflammation  Lumbar vertebrae  Pain
 
引用本文,请按以下格式著录参考文献:
中文格式:刘建,叶玉军,刘树民,刘爽.基于p38MAPK信号通路分析咪达唑仑对腰椎间盘突出症模型大鼠疼痛的影响[J].中国骨伤,2023,36(1):55~60
英文格式:LIU Jian,YE Yu-jun,LIU Shu-min,LIU Shuang.Analysis of the effect of midazolam on pain in a rat model of lumbar disc herniation based on the p38 MAPK signaling pathway[J].zhongguo gu shang / China J Orthop Trauma ,2023,36(1):55~60
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