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Repurposing of the β-Lactam Antibiotic, Ceftriaxone for Neurological Disorders: A Review

机译:改变β-内酰胺抗生素,头孢曲松钠治疗神经系统疾病的研究进展

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So far there is no cure or disease-modifying agents available for most of the well-known neurological disorders and therapy is typically focused on relieving symptoms and supportive care to improve the quality of life of the patients. Besides, the traditional de novo drug discovery technique, particularly for neurological disorders, is more challenging hence repurposing of existing drugs for these conditions are supposed to be an efficient and dynamic approach that can substantially reduce the investment spent during drug development. Currently, there is emerging evidence that suggests the potential of a beta-lactam antibiotic, ceftriaxone to alleviate the symptoms of different experimentally-induced neurological disorders, such as Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, epileptic-seizure, brain ischemia, traumatic brain injuries, and neuropathic pain. Ceftriaxone also affects the markers of oxidative status and neuro-inflammation, glutamatergic systems as well as various aggregated toxic proteins involved in the pathogenesis of different neurological disorders. Moreover, ceftriaxone administration to animal models of drug dependency was found to improve the withdrawal symptoms upon drug discontinuation. Thus, this review aimed to describe the effects of ceftriaxone against multiple models of neurological illnesses, drug dependency, and withdrawal. It also emphasizes the possible mechanisms of neuroprotective actions of ceftriaxone with respective neurological maladies.
机译:迄今为止,对于大多数众所周知的神经系统疾病,还没有治愈或疾病改良剂,并且治疗通常集中在缓解症状和支持治疗以改善患者的生活质量上。此外,传统的从头药物发现技术,尤其是针对神经系统疾病的药物发现技术,更具挑战性,因此针对这些情况重新利用现有药物被认为是一种有效且动态的方法,可以大大减少药物开发过程中的投资。目前,有新出现的证据表明,β-内酰胺类抗生素头孢曲松有可能缓解不同实验引起的神经系统疾病的症状,例如帕金森氏病,阿尔茨海默氏病,肌萎缩性侧索硬化症,癫痫发作,脑缺血,创伤性脑损伤和神经性疼痛。头孢曲松还影响氧化状态和神经炎症,谷氨酸能系统以及与各种神经系统疾病的发病机理有关的各种聚集的毒性蛋白的标志物。此外,发现头孢曲松对药物依赖性动物模型的给药改善了停药后的戒断症状。因此,本综述旨在描述头孢曲松对神经疾病,药物依赖性和戒断的多种模型的影响。它还强调了头孢曲松与相应神经系统疾病的神经保护作用的可能机制。

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