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水通道蛋白 4 和内源性大麻素系统:脑损伤的潜在治疗靶点。

Aquaporin 4 and the endocannabinoid system: a potential therapeutic target in brain injury.

机构信息

División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Coyoacán, Apartado Postal 70-253, 04510, Ciudad de Mexico, México.

出版信息

Exp Brain Res. 2024 Sep;242(9):2041-2058. doi: 10.1007/s00221-024-06896-7. Epub 2024 Jul 23.

DOI:10.1007/s00221-024-06896-7
PMID:39043897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11306651/
Abstract

Brain edema is a critical complication arising from stroke and traumatic brain injury (TBI) with an important impact on patient recovery and can lead to long-term consequences. Therapeutic options to reduce edema progression are limited with variable patient outcomes. Aquaporin 4 (AQP4) is a water channel that allows bidirectional water diffusion across the astrocyte membrane and participates in the distinct phases of cerebral edema. The absence or inhibition of this channel has been demonstrated to ameliorate edema and brain damage. The endocannabinoid system (ECS) is a neuromodulator system with a wide expression in the brain and its activation has shown neuroprotective properties in diverse models of neuronal damage. This review describes and discusses the major features of ECS and AQP4 and their role during brain damage, observing that ECS stimulation reduces edema and injury size in diverse models of brain damage, however, the relationship between AQP4 expression and dynamics and ECS activation remains unclear. The research on these topics holds promising therapeutic implications for the treatment of brain edema following stroke and TBI.

摘要

脑水肿是中风和创伤性脑损伤(TBI)的一种严重并发症,对患者的康复有重要影响,并可能导致长期后果。目前治疗脑水肿进展的方法有限,患者的预后也各不相同。水通道蛋白 4(AQP4)是一种允许水分子在星形胶质细胞膜内双向扩散的水通道,参与脑水肿的不同阶段。已有研究表明,该通道的缺失或抑制可减轻脑水肿和脑损伤。内源性大麻素系统(ECS)是一种神经调质系统,在大脑中有广泛的表达,其激活已在多种神经元损伤模型中显示出神经保护特性。本综述描述并讨论了 ECS 和 AQP4 的主要特征及其在脑损伤中的作用,观察到 ECS 刺激可减少多种脑损伤模型中的脑水肿和损伤体积,但 AQP4 表达和动力学与 ECS 激活之间的关系尚不清楚。这些研究为中风和 TBI 后脑水肿的治疗提供了有前景的治疗意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/b851bfa4d212/221_2024_6896_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/76e5455de146/221_2024_6896_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/87c17e72b1d3/221_2024_6896_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/b851bfa4d212/221_2024_6896_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/76e5455de146/221_2024_6896_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/87c17e72b1d3/221_2024_6896_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc83/11306651/b851bfa4d212/221_2024_6896_Fig3_HTML.jpg

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