| 赵 静,朱利娟,付华君,刘荣林,王亚亚.不同剂量右美托咪定治疗对大鼠术后神经功能及Keap1/Nrf2/ARE信号通路的影响[J].现代生物医学进展英文版,2023,(15):2832-2836. |
| 不同剂量右美托咪定治疗对大鼠术后神经功能及Keap1/Nrf2/ARE信号通路的影响 |
| Effects of Different Dosages of Dexmedetomidine on Postoperative Nerve Function and Keap1/Nrf2/ARE Signal Pathway in Rats |
| Received:February 05, 2023 Revised:February 28, 2023 |
| DOI：10.13241/j.cnki.pmb.2023.15.006 |
| 中文关键词: 脑缺血再灌注 右美托咪定 神经功能 Keap1/Nrf2/ARE信号通路 |
| 英文关键词: Cerebral ischemia reperfusion Dextrmetomidine Nerve function Keap1/Nrf2/ARE signal path |
| 基金项目:陕西省重点研发计划项目（2022SF-264） |
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| 中文摘要: |
| 摘要 目的：探讨不同剂量右美托咪定治疗对大鼠术后神经功能及Keap1/Nrf2/ARE信号通路的影响。方法：60只SD大鼠随机分为假手术组（n=12）、脑缺血再灌注组（n=12）、低剂量右美托咪定组（n=12）、中剂量右美托咪定组（n=12）、高剂量右美托咪定组（n=12），建立脑缺血模型，开展前瞻性研究。假手术组仅接受假手术而不造成脑缺血，术中持续静脉泵注生理盐水；脑缺血再灌注组维持脑缺血片刻，缺血即刻持续静脉泵注生理盐水；低、中、高剂量右美托咪定组脑缺血即刻静脉输注右美托咪定，首次剂量分别为6 μg/kg、60 μg/kg、600 μg/kg，剩余剂量分别以0.05 μg/kg/min、0.5 μg/kg/min、5 μg/kg/min持续静脉泵注。比较各组大鼠神经功能、炎症因子水平、氧化应激指标及Keap1/Nrf2/ARE表达。结果：与假手术组相比，低剂量右美托咪定组、中剂量右美托咪定组、高剂量右美托咪定组、脑缺血再灌注组Longa评分依次升高；与脑缺血再灌注组相比，低剂量右美托咪定组、中剂量右美托咪定组、高剂量右美托咪定组脑梗死体积、脑梗死体积所占百分比依次升高（P<0.05）。与假手术组相比，低剂量右美托咪定组、中剂量右美托咪定组、高剂量右美托咪定组、脑缺血再灌注组白介素6（IL-6）、白介素1β（IL-1β）、肿瘤坏死因子-α（TNF-α）水平依次升高（P<0.05）。与假手术组相比，低剂量右美托咪定组、中剂量右美托咪定组、高剂量右美托咪定组、脑缺血再灌注组神经元特异性烯醇化酶（NSE）、丙二醛（MDA）水平依次升高，超氧化物歧化酶（SOD）水平依次降低（P<0.05）。与假手术组相比，低剂量右美托咪定组、中剂量右美托咪定组、高剂量右美托咪定组、脑缺血再灌注组Keap1/Nrf2/ARE表达依次降低（P<0.05）。结论：低剂量右美托咪定能够保护脑缺血再灌注大鼠术后神经功能，主要通过减轻炎症反应和氧化应激来起作用，其作用机制可能与激活Keap1/Nrf2/ARE信号通路有关。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of different doses of dexmedetomidine on the postoperative nerve function and the signal pathway of Keap1/Nrf2/ARE in rats. Methods: Sixty SD rats were randomly divided into sham operation group (n=12), cerebral ischemia reperfusion group (n=12), low-dose dexmedetomidine group (n=12), medium-dose dexmedetomidine group (n=12), and high-dose dexmedetomidine group (n=12) to establish cerebral ischemia model. In the sham operation group, only sham operation was performed without cerebral ischemia, and normal saline was continuously pumped intravenously during the operation; In the cerebral ischemia reperfusion group, the cerebral ischemia was maintained for a moment, and the normal saline was continuously pumped intravenously immediately after ischemia; In the low, medium and high dose dexmedetomidine group, the first dose of dexmedetomidine was 6 μg/kg, 60 μg/kg, 600 μg/kg, the remaining dose is 0.05 μg/kg/min, 0.5 μg/kg/min, 5 μg/kg/min continuous intravenous infusion. The nerve function, inflammatory factor level, oxidative stress index and the expression of Keap1/Nrf2/ARE were compared in each group. Results: Compared with the sham operation group, the Longa scores of low-dose dexmedetomidine group, medium-dose dexmedetomidine group, high-dose dexmedetomidine group and cerebral ischemia reperfusion group increased in turn; Compared with the cerebral ischemia reperfusion group, the volume of cerebral infarction and the percentage of cerebral infarction volume in the low-dose dexmedetomidine group, the middle-dose dexmedetomidine group and the high-dose dexmedetomidine group increased in turn (P<0.05). Compared with sham operation group, low-dose dexmedetomidine group, medium-dose dexmedetomidine group, high-dose dexmedetomidine group, cerebral ischemia reperfusion group, interleukin-6 (IL-6), interleukin-1β (IL-1 β), Tumor necrosis factor- α (TNF-α) The levels increased in turn (P<0.05). Compared with the sham-operated group, the levels of neuron specific enolase (NSE) and malondialdehyde (MDA) in the low-dose dexmedetomidine group, the medium-dose dexmedetomidine group, the high-dose dexmedetomidine group and the cerebral ischemia-reperfusion group increased in turn, and the levels of superoxide dismutase (SOD) decreased in turn (P<0.05). Compared with the sham-operated group, the expression of Keap1/Nrf2/ARE in the low-dose dexmedetomidine group, the medium-dose dexmedetomidine group, the high-dose dexmedetomidine group, and the cerebral ischemia-reperfusion group decreased in turn (P<0.05). Conclusion: Low-dose dexmedetomidine can protect the neurological function of rats after cerebral ischemia reperfusion, mainly by reducing inflammatory reaction and oxidative stress, and its mechanism may be related to the activation of Keap1/Nrf2/ARE signal pathway. |
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