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Biochem Biophys Res Commun. 2016 Sep 16;478(2):553-8. doi: 10.1016/j.bbrc.2016.07.098. Epub 2016 Jul 25.

Glycyrrhizic acid prevents astrocyte death by neuromyelitis optica-specific IgG via inhibition of C1q binding.

Author information

1
Department of Neurology, Korea University Guro Hospital, Seoul, Republic of Korea.
2
Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea.
3
Department of Anatomy, Inha University School of Medicine, Inchon, Republic of Korea.
4
Laboratory Animal Center, Daegu-Gyeongbuk Medical Innovation Foundation, Republic of Korea.
5
Convergence Research Center for Dementia, Korea Institute of Science and Technology, Seoul, Republic of Korea; Department of Biological Chemistry, University of Science and Technology, Daejeon, Republic of Korea. Electronic address: kdpark@kist.re.kr.
6
Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea. Electronic address: sueh916@gmail.com.

Abstract

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system and is mediated by complement-dependent cytotoxicity (CDC) of NMO-specific immunoglobulin G (IgG) antibodies (NMO-IgG). Glycyrrhizic acid (GA) has numerous pharmacological effects including inhibition of the complement pathway. We aimed to study the influence of GA on NMO-IgG-induced CDC. NMO-IgG samples from 7 patients with NMO, together with human complement, induced CDC in an aquaporin 4 M23-overexpressing glial cell line, an in vitro NMO model. GA attenuated NMO-IgG-induced CDC in a dose-dependent manner. The mechanism of the GA-related CDC inhibition was sequentially dissected and found to involve inhibition of C1q binding to NMO-IgG. Consequently, GA attenuates NMO-IgG-induced CDC and may be a promising novel therapeutic agent against NMO.

KEYWORDS:

Complement dependent cytotoxicity; Glycyrrhizic acid; Neuromyelitis optica

PMID:
27462020
DOI:
10.1016/j.bbrc.2016.07.098
[Indexed for MEDLINE]

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