reduced DSS-induced colitis and anxiety-like behavior in mice, apparently through microbiota-linked and glial inflammatory signaling.
Evidence
Preclinical mouse experiments used dextran sodium sulfate colitis with behavioral, hippocampal, microbiome, metabolite, inositol supplementation, and inhibitor readouts.
Caveat
The findings are from a mouse model and mechanistic manipulations, so they do not show clinical benefit for people with IBD.
Simplified
The gut-brain axis links gut inflammation to psychiatric symptoms in inflammatory bowel disease (IBD), but the underlying mechanisms remain unclear. We demonstrate that neuropeptide (SP) alleviated intestinal injury and behavioral disorders induced by dextran sodium sulfate in mice. SP mitigated hippocampal neuroinflammation and inhibited microglial activation and astrocyte loss. Furthermore, SP improved gut microbiome dysregulation, and its protective effects depended on the putative roles of microbiota. Notably, through modulating microbiota, SP dampened the NF-κB pathway in microglia, and increased GABAergic/Casignaling within astrocytes. SP elevated the microbiota-derived metabolite . Supplementing inositol mimicked SP's benefits and activated GABAergic signaling, while the inositol inhibitor reversed SP's neuroprotective impacts, highlighting inositol's indispensable role. Collectively, SP exerts beneficial effects via microbiota's putative roles and inositol, involving the suppression of microglial NF-κB pathway while enhancing astrocytic GABAergic/Ca²⁺ signaling. Our findings underscore SP's potential as a therapeutic intervention for these disorders in IBD. 2+
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Gut-Brain Axis