Magnolia officinalis bark extract improves depressive-like behavior in DSS-induced colitis mice

Abstract

Most studies on the pathogenesis of inflammatory bowel disease (IBD) focus on gut function damage and gastrointestinal symptoms; however, psychiatric disorders, including depression and anxiety, have also been recognized as significant causes. Recently, we reported that Magnolia officinalis bark extract (MBE) alleviated enterocyte death in dextran sulfate sodium (DSS)-induced colitis mouse model that mimics IBD; however, the therapeutic effects of MBE on neurological symptoms and underlying mechanisms of IBD remain unclear. In this study, we aimed to elucidate the mechanisms by which microglia and astrocytes improve MBE-induced depression and anxiety. We found that MBE treatment improved DSS-induced weight loss, colon-length shortening, and cell death, with ameliorateon of depression/anxiety-like behavioral disorders. Systemic treatment with MBE significantly decreased DSS-induced proliferation of microglia and astrocytes in the hippocampal region, and attenuated the increase in pro-inflammatory cytokines, including IL-6 and COX-2. Interestingly, MBE alleviated DSS-induced alterations of the serotonergic system by improving serotonin levels, and expression of serotonin 4 receptor (5-HT4R) and cAMP response element-binding protein (CREB) phosphorylation in the hippocampus. Overall, our findings indicate that MBE exerts protective effects not only on gastrointestinal function but also on neuropsychiatric disorders caused by colitis, which may be developed to treat IBD.