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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.

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Department of Neurology, Korea University Guro Hospital, Seoul, Republic of Korea.
Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea.
Department of Anatomy, Inha University School of Medicine, Inchon, Republic of Korea.
Laboratory Animal Center, Daegu-Gyeongbuk Medical Innovation Foundation, Republic of Korea.
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:
Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea. Electronic address:


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.


Complement dependent cytotoxicity; Glycyrrhizic acid; Neuromyelitis optica

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