Adropin可能通过降低NF-κB/IkB-α信号通路的激活,改善戊四唑诱导的大鼠癫痫发作模型中的行为性癫痫发作以及相关的神经炎症、氧化应激和神经损伤。

IF 3.5 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Shaafah Namulodi, Ibrahim Ethem Torun, Fahri Bayiroglu, Mehmet Salih Kaya, Erkan Kilinc
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引用次数: 0

摘要

本研究旨在探讨adropin对戊四唑(PTZ)诱导大鼠癫痫发作的影响,包括癫痫发作活动、神经炎症、氧化应激和认知功能。雄性Wistar大鼠随机分为6组,每组7只,分别为对照组、PTZ组、adropin(2µg/kg或10µg/kg) + PTZ组、L-NAME组+ adropin + PTZ组、丙戊酸组+ PTZ组。阳性对照给予抗惊厥药物丙戊酸。非选择性一氧化氮合酶抑制剂L-NAME与adropin联合使用,以阐明adropin是否通过一氧化氮途径发挥其可能的作用。评估行为性癫痫发作、神经炎症及相关通路生化指标、氧化应激、认知功能和神经存活/损伤。Adropin(10µg/kg)降低了pz诱导的癫痫发作的严重程度和持续时间,减轻了皮质和海马的促炎(IL-1β、IL-6、TNF-α和相关转录因子pNF-κB-p65和pIκBα)、氧化(MDA)和神经损伤(GFAP)标志物,同时提高了抗炎(IL-10)、抗氧化(SOD)和神经存活(BDNF)标志物。adropin和L-NAME联合使用也表现出与单独使用adropin相似的效果。换句话说,阻断全身一氧化氮的产生并不能改变adropin的作用。然而,adropin并没有显著改善被动回避测试中的认知表现。丙戊酸作为阳性对照,逆转了ptz诱导的效应。这些发现表明,adropin可能通过调节NF-κB/IkB-α信号传导,在ptz诱导的癫痫模型中具有抗惊厥、抗炎、抗氧化和神经保护作用。因此,adropin可能是一个多方面和有前途的药物,在预防和治疗癫痫发作的未来。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Adropin ameliorates behavioral seizures and the relevant neuroinflammation, oxidative stress, and neural damage in a rat model of pentylenetetrazole-induced seizure potentially by reducing the activation of NF-κB/IkB-α signaling pathway.

Adropin ameliorates behavioral seizures and the relevant neuroinflammation, oxidative stress, and neural damage in a rat model of pentylenetetrazole-induced seizure potentially by reducing the activation of NF-κB/IkB-α signaling pathway.

Adropin ameliorates behavioral seizures and the relevant neuroinflammation, oxidative stress, and neural damage in a rat model of pentylenetetrazole-induced seizure potentially by reducing the activation of NF-κB/IkB-α signaling pathway.

Adropin ameliorates behavioral seizures and the relevant neuroinflammation, oxidative stress, and neural damage in a rat model of pentylenetetrazole-induced seizure potentially by reducing the activation of NF-κB/IkB-α signaling pathway.

This study aimed to investigate the effects of adropin on seizure activity, neuroinflammation, oxidative stress, and cognitive function in a rat model of pentylenetetrazole (PTZ)-induced seizure. Male Wistar rats were randomly assigned to six groups (n = 7/each group), as follows: control, PTZ, adropin (2 µg/kg or 10 µg/kg) + PTZ, L-NAME + adropin + PTZ, and valproic acid + PTZ groups. Anticonvulsant medicine valproic acid was administered as positive control. Non-selective nitric oxide synthase inhibitor L-NAME was administered together with adropin to elucidate whether adropin exerts its possible effects through the nitric oxide pathway. Behavioral epileptic seizures, biochemical markers of neuroinflammation and relevant pathway, oxidative stress, cognitive function and neural survival/damage were assessed. Adropin (10 µg/kg) reduced PTZ-induced seizure severity and duration, and mitigated cortical and hippocampal pro-inflammatory (IL-1β, IL-6, TNF-α and related transcription factors pNF-κB-p65 and pIκBα), oxidant (MDA) and neural damage (GFAP) markers while elevating anti-inflammatory (IL-10), antioxidant (SOD) and neural survival (BDNF) markers. Combining adropin and L-NAME also exhibited similar effects to adropin alone. In other words, blocking systemic nitric oxide production did not alter the effects of adropin. However, adropin did not significantly improve cognitive performance in the passive avoidance test. Valproic acid, as a positive control, reversed the PTZ-induced effects. These findings suggest that adropin exhibits anticonvulsant, anti-inflammatory, antioxidant and neuroprotective properties in PTZ-induced seizure model potentially through modulation of NF-κB/IkB-α signalling. Therefore, adropin may be a multi-faceted and promising agent in the prevention and management of epileptic seizures in the future.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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