title: Glycyrol suppresses collagen-induced arthritis by regulating autoimmune and inflammatory responses.
abstract: Glycyrol is a natural compound extracted from Glycyrrhiza uralensis, first reported by us to be a new immunosuppressant. Here, we demonstrate its beneficial effect in collagen-induced arthritis (CIA) in mice, a model for rheumatoid arthritis (RA) in man, and we document the underlying mechanisms. Peroral administration of glycyrol significantly reduced clinical scores, alleviated cartilage and bone erosion and reduced levels of serum inflammatory cytokines. Glycyrol also decreased delayed-type hypersensitivity, improved carbon clearance and reduced acetic acid-induced capillary permeability. Furthermore, glycyrol decreased NF-κB and NFAT transcriptional activities and inhibited IL-2 expression. The therapeutic effect of glycyrol was associated with down-regulation of both autoimmune and inflammatory reactions. In addition, we demonstrated that glycyrol has minimal acute toxicity in mice. Therefore, we propose that glycyrol may hold promise for future treatment of RA.
authors.affiliation: Department of Biochemistry and Molecular Biology, Beijing Normal University, Gene Engineering and Biotechnology Beijing Key Laboratory, Beijing, P. R. of China.
authors.forename: Yanxia
authors.initials: Y
authors.lastname: Fu
authors.affiliation: Department of Biochemistry and Molecular Biology, Beijing Normal University, Gene Engineering and Biotechnology Beijing Key Laboratory, Beijing, P. R. of China.
authors.forename: Hailing
authors.initials: H
authors.lastname: Zhou
authors.affiliation: Department of Biochemistry and Molecular Biology, Beijing Normal University, Gene Engineering and Biotechnology Beijing Key Laboratory, Beijing, P. R. of China.
authors.forename: Shuangyan
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Biochemistry and Molecular Biology, Beijing Normal University, Gene Engineering and Biotechnology Beijing Key Laboratory, Beijing, P. R. of China.
authors.forename: Qun
authors.initials: Q
authors.lastname: Wei
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use* / Q000633:toxicity; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use* / Q000633:toxicity; D001169:Arthritis, Experimental / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D002199:Capillary Permeability / Q000187:drug effects; D002358:Cartilage, Articular / Q000473:pathology; D016207:Cytokines / Q000097:blood; D015536:Down-Regulation / Q000187:drug effects; D004353:Drug Evaluation, Preclinical; D005419:Flavonoids / Q000494:pharmacology / Q000627:therapeutic use* / Q000633:toxicity; D006968:Hypersensitivity, Delayed / Q000188:drug therapy; D007166:Immunosuppressive Agents / Q000494:pharmacology / Q000627:therapeutic use* / Q000633:toxicity; D007249:Inflammation; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics; D008264:Macrophages / Q000187:drug effects / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008811:Mice, Inbred DBA; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D050778:NFATC Transcription Factors / Q000037:antagonists & inhibitors / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects; D008517:Phytotherapy; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D018501:Antirheumatic Agents; D016207:Cytokines; D005419:Flavonoids; D007166:Immunosuppressive Agents; D007376:Interleukin-2; D016328:NF-kappa B; D050778:NFATC Transcription Factors; C531349:glycyrol