Apelin-13 reduces lipopolysaccharide-induced neuroinflammation and cognitive impairment via promoting glucocorticoid receptor expression and nuclear translocation. (25th September 2022)

• Record Type: Journal Article
• Authors: Hu, Sheng; Shen, Pei; Chen, Bin; Tian, Shao-Wen; You, Yong
• Is Part Of: Neuroscience letters. Volume 788(2022)
• Publication Date: 2022-09-25
• Subjects: Apelin-13 -- Neuroinflammation -- Cognitive decline -- Glucocorticoid receptor -- Hippocampus; LPS lipopolysaccharide -- i.c.v. intracerebroventricular -- CNS central nervous system -- GR glucocorticoid receptor -- NORT Novel object recognition test -- YMT Y maze test -- GFAP glial fibrillary acidic protein -- IBA-1 ionized calcium-binding adapter molecule-1; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2022.136850
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Apelin-13, a G protein-coupled receptor, can reduce neuroinflammation to improve cognitive of rats by lipopolysaccharide (LPS)-induced neuroinflammation. Apelin-13 improves neuroinflammation-related cognitive decline by activating GR expression and nuclear translocation in rats. The results indicate apelin-13 may serves as a potential agent in the treatment of neuroinflammation-related cognitive decline. Abstract: Neuroinflammation is usually associated with cognitive decline, which is involved in neurodegenerative diseases. Apelin, a neuropeptide, exerts various biological roles in central nervous system. Recent evidence showed that apelin-13, an active form of apelin, suppresses neuroinflammation and improves cognitive decline in diverse pathological processes. However, the underlying mechanism of apelin-13 in neuroinflammation remains largely unknown. The present study aimed to determine underlying mechanism of apelin-13 on neuroinflammation-related cognitive decline. The lipopolysaccharide (LPS) intracerebroventricular (i.c.v.) to is used to establish a rat model of neuroinflammation-related cognitive decline. The results showed that apelin-13 inhibits LPS-induced neuroinflammation and improves cognitive impairment. Apelin-13 upregulates the GR level and nuclear translocation in hippocampus of rats. Moreover, glucocorticoid receptor inhibitor RU486 prevents apelin-13-mediated neuroprotective actions on cognitive function. Taken together, apelin-13 could exert a protective effect in neuroinflammation-mediated cognitive impairment via the activation of GR expression and nuclear translocation.