Mashayekhi-Sardoo Habibeh, Razazpour Fateme, Hakemi Zohreh, Hedayati-Moghadam Mahdiyeh, Baghcheghi Yousef
Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, 7861755765, Iran.
School of Health, Jiroft University of Medical Sciences, Jiroft, Iran.
Cell Mol Neurobiol. 2025 May 22;45(1):49. doi: 10.1007/s10571-025-01569-7.
Ethanol consumption is widely recognized for its detrimental effects on mental health, particularly its association with depressive disorders. This narrative review aims to explore the intricate molecular mechanisms underlying ethanol-induced depression, synthesizing findings from preclinical and clinical studies. We begin by providing an overview of the relationship between chronic ethanol consumption and depression, highlighting compelling evidence from diverse populations. Subsequently, we delve into insights from animal models that elucidate the pathophysiological changes triggered by prolonged ethanol exposure. Key mechanisms identified include oxidative stress, which contributes to cellular damage; neuroinflammation, characterized by the activation of glial cells and altered cytokine profiles; and disruptions in neurotrophic factors that impair neuronal growth and survival. Furthermore, we discuss the induction of apoptosis in neural cells and the significant impact of ethanol on neurotransmitter receptor remodeling and regulation, leading to altered synaptic transmission. While substantial progress has been made in understanding these mechanisms, we also acknowledge the limitations of current research methodologies and call for further investigations to translate these findings into effective therapeutic strategies for individuals affected by ethanol-induced depression. This review ultimately underscores the need for a comprehensive understanding of the molecular underpinnings of ethanol's impact on mood disorders, paving the way for improved interventions and preventative measures.
乙醇消费对心理健康的有害影响已得到广泛认可，尤其是其与抑郁症的关联。本叙述性综述旨在探讨乙醇诱发抑郁症背后复杂的分子机制，综合临床前和临床研究的结果。我们首先概述慢性乙醇消费与抑郁症之间的关系，强调来自不同人群的有力证据。随后，我们深入探讨动物模型的见解，这些见解阐明了长期乙醇暴露引发的病理生理变化。确定的关键机制包括导致细胞损伤的氧化应激；以胶质细胞激活和细胞因子谱改变为特征的神经炎症；以及损害神经元生长和存活的神经营养因子的破坏。此外，我们讨论神经细胞凋亡的诱导以及乙醇对神经递质受体重塑和调节的重大影响，导致突触传递改变。虽然在理解这些机制方面取得了重大进展，但我们也承认当前研究方法的局限性，并呼吁进一步开展研究，将这些发现转化为针对受乙醇诱发抑郁症影响的个体的有效治疗策略。本综述最终强调需要全面了解乙醇对情绪障碍影响的分子基础，为改进干预措施和预防措施铺平道路。
