18β-Glycyrrhetinic acid alleviates demyelination by modulating the microglial M1/M2 phenotype in a mouse model of cuprizone-induced demyelination. (11th June 2021)

• Record Type: Journal Article
• Authors: Tian, Hui; Cheng, Yahong; Zhang, Yiyuan; Bai, Xinying; Jiang, Yuan; Li, Jinjin; Fan, Shiqi; Ding, Hong
• Is Part Of: Neuroscience letters. Volume 755(2021)
• Publication Date: 2021-06-11
• Subjects: CPZ cuprizone -- LFB luxol-fast blue -- MBP myelin basic protein -- MS multiple sclerosis -- CNS central nervous system -- 18β-GA 18β-glycyrrhetinic acid -- GL glycyrrhizin -- CMC-Na sodium carboxyl methyl cellulose -- OFT open-field test -- PFA paraformaldehyde -- PBS phosphate buffered saline; 18β-Glycyrrhetinic acid -- Demyelination -- Cuprizone -- M1/M2 phenotype; 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.2021.135871
• Languages: English
• ISSNs: 0304-3940

Abstract

Graphical abstract: Highlights: 18β-GA (a constituent of licorice) effectively reversed the mice behavioral dysfunction after exposure to cuprizone for five weeks. 18β-GA sufficiently alleviates demyelination in a mouse model of cuprizone-induced demyelination. The function of 18β-GA is related to moderating M1/M2 polarisation. Abstract: This research aimed to examine the nutritious supplementary function of 18β-Glycyrrhetinic acid (18β-GA) in moderating the myelin sheath destruction and behavioral impairments observed in the cuprizone model of demyelination. Mice were fed daily on food containing cuprizone (0.3 %) and given doses of 18β-GA (5 or 1 mg/kg) for a period of five weeks. The groups treated with 18β-GA exhibited improvements in exploratory behavior, locomotive activity, and weight. As assessed using luxol-fast blue and myelin basic protein (MBP) staining, which were used to detect demyelination in the brain, 18β-GA both reduced and prevented instances of cuprizone-induced demyelinating lesions; treatment with 18β-GA also caused the MBP level in the corpus callosum to increase. Furthermore, alongside these positive results following 18β-GA treatment, microglial polarisation was also observed to shift towards the beneficial M2 phenotype. The results of this research thus indicate the potential clinical application of 18β-GA for the prevention of myelin damage and behavioral dysfunction.