Therapeutic effect of baicalin on experimental autoimmune encephalomyelitis is mediated by SOCS3 regulatory pathway

• DOI: 10.1038/srep17407
• Publication Date: 2015-11-30T12:38:12Z
• Authors: Yuan Zhang; Xing Li; Bogoljub Ciric; Cun-Gen Ma; Bruno Gran; Abdolmohamad Rostami; Guang-Xian Zhang
• Keywords: Flavonoids; 0301 basic medicine; Encephalomyelitis, Autoimmune, Experimental; Multiple Sclerosis; Anti-Inflammatory Agents, Non-Steroidal; NF-kappa B; Cell Differentiation; Suppressor of Cytokine Signaling Proteins; Th1 Cells; Lymphocyte Activation; Article; 3. Good health; Disease Models, Animal; Mice; STAT Transcription Factors; 03 medical and health sciences; Suppressor of Cytokine Signaling 3 Protein; T-Lymphocyte Subsets; Animals; Cytokines; Th17 Cells; Female; Inflammation Mediators; Signal Transduction

AbstractNatural compounds derived from medicinal plants have long been considered a rich source of novel therapeutic agents. Baicalin (Ba) is a bioactive flavonoid compound derived from the root of Scutellaria baicalensis, an herb widely used in traditional medicine for the treatment of various inflammatory diseases. In this study, we investigate the effects and mechanism of action of Ba in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Ba treatment effectively ameliorated clinical disease severity in myelin oligodendrocyte glycoprotein (MOG)35–55 peptide-induced EAE and reduced inflammation and demyelination of the central nervous system (CNS). Ba reduced infiltration of immune cells into the CNS, inhibited expression of proinflammatory molecules and chemokines and prevented Th1 and Th17 cell differentiation via STAT/NFκB signaling pathways. Further, we showed that SOCS3 induction is essential to the effects of Ba, given that the inhibitory effect of Ba on pathogenic Th17 responses was largely abolished when SOCS3 signaling was knocked down. Taken together, our findings demonstrate that Ba has significant potential as a novel anti-inflammatory agent for therapy of autoimmune diseases such as MS.