神经炎症被识别为中枢神经系统中显著的炎症反应。脂多糖（Lipopolysaccharide，LPS）刺激先天免疫反应，并被用作体内动物模型来研究炎症。甲氧氯普胺（Meclizine，MCLZ）是一种组胺拮抗剂，具有潜在的神经保护性能。将40只成年雄性瑞士白种大鼠分为四组（每组n = 10）。第1组作为阴性对照组。第2至4组被注射LPS（5 mg/kg；i.p）。第2组作为LPS对照组。第3、4组分别口服MCLZ（12.5、25 mg/kg）14天。LPS给药导致小鼠出现明显的神经炎症，表现为显著的炎症组织病理学变化和阳性的神经胶质酸性蛋白（Glial Fibrillary Acidic Protein，GFAP）免疫组织化学染色，同时伴随大脑组织内白细胞介素-1β（Interleukin-1-beta，IL-1β）、肿瘤坏死因子-α（Tumor Necrosis Factor-alpha，TNF-α）、核因子-κβ（Nuclear Factor Kappa-Beta，NF-κβ）、蛋白激酶B（Protein Kinase B，AKT）、细胞外信号调节激酶（Extracellular Signal-Regulated Kinase，ERK）和C-Jun N-terminal Kinases（JNK）的显著升高。MCLZ治疗显著降低小鼠脑中的上述所有指标。此外，MCLZ治疗改善了脑组织中的炎症组织病理学变化和GFAP免疫染色。本研究首次确定了MCLZ对LPS诱导的小鼠神经炎症的保护性抗炎效应。MCLZ通过改善炎症组织病理学变化以及神经胶质酸性蛋白免疫染色，并下调AKT/NF-κβ/ERK/JNK信号通路来保护免受神经炎症的侵害。预期MCLZ将成为神经炎症治疗方案中的潜在保护性候选药物。© 2023. 作者（们）。

Neuroinflammation is identified as significant inflammatory reactions occurring in the central nervous system. Lipopolysaccharide (LPS) stimulates innate immune reactions and is used as an in vivo animal model for the investigation of inflammation. Meclizine (MCLZ) is a histamine antagonist with potential neuroprotective qualities. Forty adult male Swiss albino mice were divided into four groups (n = 10). Group 1 served as a control negative group. Groups 2-4 were injected with LPS (5 mg/kg; i.p). Group 2 served as LPS-control. Groups 3 & 4 were given MCLZ (12.5 & 25 mg/kg; p.o) respectively for 14 days. LPS administration resulted in significant neuroinflammation in mice as was revealed by significant inflammatory histopathological changes and positive immunohistochemical staining of glial fibrillary acidic proteins (GFAP) accompanied by significant elevations of brain tissue contents of interleukin-1-beta (IL-1β), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa-beta (NF-κβ), protein kinase B (AKT), extracellular signal-regulated kinase (ERK) and C-Jun N-Terminal Kinases (JNK). MCLZ treatment significantly down-regulated all the aforementioned parameters in mice brains. Moreover, MCLZ treatment ameliorated the inflammatory histopathological changes and GFAP immunostaining in brain tissues. The current study identifies for the first time the protective anti-neuroinflammatory effects of MCLZ against LPS-induced neuroinflammation in mice. MCLZ protected against neuroinflammation via the amelioration of inflammatory histopathological changes as well as neuronal GFAP immunostaining and down-regulated the AKT/NF-κβ/ERK/JNK signaling pathway. MCLZ is anticipated as a potential protective candidate for the addition to the treatment protocol of neuroinflammation.© 2023. The Author(s).