Kim Ji-Sun, Cheon Soyoung, Kim Seung Woo, Kim Boram, Kim Heejaung, Park Ki Duk, Kim Sung-Min
Department of Neurology, Korea University Guro Hospital, Seoul, Republic of Korea.
Department of Neurology, Seoul National University Hospital, Seoul, Republic of Korea.
Biochem Biophys Res Commun. 2016 Sep 16;478(2):553-8. doi: 10.1016/j.bbrc.2016.07.098. Epub 2016 Jul 25.
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.
视神经脊髓炎（NMO）是一种中枢神经系统炎性脱髓鞘疾病，由NMO特异性免疫球蛋白G（IgG）抗体（NMO-IgG）介导的补体依赖性细胞毒性（CDC）引起。甘草酸（GA）具有多种药理作用，包括抑制补体途径。我们旨在研究GA对NMO-IgG诱导的CDC的影响。来自7例NMO患者的NMO-IgG样本与人补体一起，在水通道蛋白4 M23过表达的胶质细胞系（一种体外NMO模型）中诱导CDC。GA以剂量依赖性方式减弱NMO-IgG诱导的CDC。对GA相关的CDC抑制机制进行了逐步剖析，发现其涉及抑制C1q与NMO-IgG的结合。因此，GA减弱NMO-IgG诱导的CDC，可能是一种有前景的新型抗NMO治疗药物。
