It has been well recognized that prolactin (PRL), a pleiotropic hormone, has many functions in the brain, such as maternal behavior, neurogenesis, and neuronal plasticity, among others. Recently, it has been reported to have a significant role in neuroprotection against excitotoxicity. Glutamate excitotoxicity is a common alteration in many neurological and neurodegenerative diseases, leading to neuronal death. In this sense, several efforts have been made to decrease the progression of these pathologies. Despite various reports of PRL’s neuroprotective effect against excitotoxicity, the signaling pathways that underlie this mechanism remain unclear. This review aims to describe the most recent and relevant studies on the molecular signaling pathways, particularly, PI3K/AKT, NF-κB, and JAK2/STAT5, which are currently under investigation and might be implicated in the molecular mechanisms that explain the PRL effects against excitotoxicity and neuroprotection. Remarkable neuroprotective effects of PRL might be useful in the treatment of some neurological diseases.

众所周知，催乳素 (PRL) 是一种多效激素，在大脑中具有许多功能，例如母性行为、神经发生和神经元可塑性等。最近，据报道它在对抗兴奋性毒性的神经保护中具有重要作用。谷氨酸兴奋性毒性是许多神经和神经退行性疾病的常见改变，导致神经元死亡。从这个意义上说，已经做出了一些努力来减少这些病理的进展。尽管有各种关于 PRL 对兴奋性毒性的神经保护作用的报道，但作为这种机制基础的信号通路仍不清楚。本综述旨在描述关于分子信号通路的最新和相关研究，特别是 PI3K/AKT、NF-κB 和 JAK2/STAT5，目前正在研究中，可能与解释 PRL 对兴奋性毒性和神经保护作用的分子机制有关。PRL 的显着神经保护作用可能有助于治疗某些神经系统疾病。