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丁丙诺啡对大鼠中度创伤性脑损伤的疗效。

The efficacy of buprenorphine on moderate traumatic brain injury in the rat model.

机构信息

Trauma Research Center, Clinical Sciences Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran.

Department of Medicine Genetic, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran.

出版信息

Neurol Res. 2023 Nov;45(11):1055-1062. doi: 10.1080/01616412.2023.2257447. Epub 2023 Sep 11.

DOI:10.1080/01616412.2023.2257447
PMID:37695813
Abstract

INTRODUCTION

Traumatic brain injury (TBI) is the leading cause of death, disability, and mental health disorders. A wide range of bioactive lipids, cytokines, and chemokines drives the inflammatory response. This study aimed to assess the efficacy of buprenorphine on moderate Trauma Brain Injury (mTBI) in rats.

METHODS

In this study, 21 Wistar male rats weighing 230 ± 10 g were included. We trained cases by Morris water navigation task and mTBI induced by the pendulum. Then, buprenorphine treatment with 0.05 mg per kilogram of body weight continued from day 8 to 21. Finally, by Micro-Computed Tomography, behavioral evaluation by the Morris aqueous riddle test and biochemical factors of inflammation were assessed.

RESULTS

Severe subdural inflammation was more in the treatment group than in the control group. The behavior of Rats showed that in the buprenorphine group, the mean duration of finding the platform increased compared to the control and Sham groups. However, the groups had no significant differences ( > 0.05). Biochemically, buprenorphine increased prolactin and decreased cortisol compared to the control and trauma groups ( < 0.05).

CONCLUSION

These results suggest that buprenorphine causes fewer changes in behavioral functions in rats' models of mTBI and, because of their positive effect changes on inflammation biomarkers, biochemical behavioral tests, and CT scan images, could be ideal analgesic agents for pre-clinical responses after TBI.

摘要

简介

创伤性脑损伤(TBI)是导致死亡、残疾和精神健康障碍的主要原因。广泛的生物活性脂质、细胞因子和趋化因子驱动炎症反应。本研究旨在评估丁丙诺啡对大鼠中度创伤性脑损伤(mTBI)的疗效。

方法

在这项研究中,纳入了 21 只 Wistar 雄性大鼠,体重为 230±10g。我们通过 Morris 水迷宫任务和摆锤诱导 mTBI 对病例进行训练。然后,从第 8 天到第 21 天,每公斤体重用 0.05 毫克丁丙诺啡进行治疗。最后,通过微计算机断层扫描、Morris 水迷宫行为评估和炎症的生化因子进行评估。

结果

治疗组比对照组有更严重的硬脑膜下炎症。大鼠的行为表明,在丁丙诺啡组中,与对照组和假手术组相比,找到平台的平均持续时间增加。然而,这些组之间没有显著差异(>0.05)。在生化方面,与对照组和创伤组相比,丁丙诺啡增加了催乳素,降低了皮质醇(<0.05)。

结论

这些结果表明,丁丙诺啡在大鼠 mTBI 模型中对行为功能的变化较小,并且由于其对炎症生物标志物、生化行为测试和 CT 扫描图像的积极影响,可能是 TBI 后临床前反应的理想镇痛剂。

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