Research Center for Addiction and Risky Behaviors (ReCARB), Iran Psychiatric Center, Iran University of Medical Sciences, Tehran, Iran.
Razi Drug Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Med Hypotheses. 2019 Mar;124:21-25. doi: 10.1016/j.mehy.2019.01.017. Epub 2019 Jan 24.
The neurodegeneration and neurobehavioral consequences of alcohol are serious and offering therapeutic approaches for management of these types of neurodegeneration is one of the main concerns of researchers in this manner. Alcohol-stimulated oxidative stress, apoptosis and inflammation, with modulation of involved signaling pathway in neuroprotection, was reported previously. Neuroprotective strategy for management of alcohol induced neurodegeneration through a new generation neuroprotective agent and based on modulation of some neuroprotective signaling pathway such as CREB/BDNF and Akt/GSK has always been superior to any other therapeutic interventions. Therefore, the introduction and development of potential new neuroprotective properties and clarification of their effects on major cell signaling such as CREB/BDNF and Akt/GSK is necessitated. During recent years, using new neuroprotective compounds with therapeutic probability for treatment of alcohol induced neuro-biochemical and neuro-behavioral malicious effects have been amazingly increased. Many previous studies have reported the neuroprotective roles of crocin (major active component of saffron) in multiple neurodegenerative events and diseases in animal model. But the role of crocin neuroprotective effects against alcohol induced neurodegeneration and neurobehavioral sequels and also role of CREB/BDNF and Akt/GSK in this manner remain unclear. Hence we hypothesized that by using crocin in alcohol dependent subject it would provide neuroprotection against alcohol induced neurodegeneration and neurobehavioral and probably can manage sequels of alcohol abuses. Also we hypothesized that crocin, via intonation of CREB/BDNF and Akt/GSK signaling pathway, can inhibit alcohol induced neurodegeneration. In this article, we tried to discuss our hypothesis regarding the possible role of crocin, as a potent neuroprotective agent, and also role of Akt/GSK and CREB/BDNF signaling pathway in treatment of alcohol induced neurodegeneration and neurobehavioral through its anti-inflammatory,anti-apoptotic, anti-oxidative stress and cognitive enhancer.
酒精导致的神经退行性变和神经行为后果严重，因此，寻找治疗这些类型的神经退行性变的方法是此类研究的主要关注点之一。先前已有研究报道，酒精刺激氧化应激、细胞凋亡和炎症，涉及神经保护的相关信号通路也发生了变化。通过新一代神经保护剂并基于调节某些神经保护信号通路（如 CREB/BDNF 和 Akt/GSK）来管理酒精诱导的神经退行性变的神经保护策略一直优于任何其他治疗干预措施。因此，需要引入和开发具有潜在神经保护特性的新方法，并阐明它们对主要细胞信号通路（如 CREB/BDNF 和 Akt/GSK）的影响。近年来，使用具有治疗潜力的新型神经保护化合物来治疗酒精引起的神经生化和神经行为不良影响的研究显著增加。许多先前的研究已经报道了藏红花酸（藏红花的主要活性成分）在动物模型中的多种神经退行性疾病中的神经保护作用。但是，藏红花酸对酒精诱导的神经退行性变和神经行为后果的神经保护作用，以及 CREB/BDNF 和 Akt/GSK 在这种情况下的作用尚不清楚。因此，我们假设在酒精依赖的个体中使用藏红花酸可以提供神经保护作用，防止酒精引起的神经退行性变和神经行为变化，并且可能可以管理酒精滥用的后果。我们还假设，藏红花酸通过调节 CREB/BDNF 和 Akt/GSK 信号通路，可以抑制酒精诱导的神经退行性变。在本文中，我们试图讨论我们的假设，即藏红花酸作为一种有效的神经保护剂，以及 Akt/GSK 和 CREB/BDNF 信号通路在治疗酒精诱导的神经退行性变和神经行为中的作用，通过其抗炎、抗细胞凋亡、抗氧化应激和认知增强作用。
