ArticleInflammopharmacology2026
Paeonia suffruticosa root bark extract alleviates gut-brain axis dysfunction in DSS-induced colitis via suppression of intestinal necroptosis and glial activation.
Article in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Intestinal mucosal inflammation and epithelial injury can be associated with central inflammatory and behavioral alterations through gut-brain axis-related pathways. This highlights the need for therapeutic strategies that target intestinal inflammatory injury while also attenuating colitis-associated central responses. Here, we evaluated the effects of Paeonia suffruticosa root bark extract (PSE) on dextran sulfate sodium (DSS)-induced colitis and associated neuroinflammatory and behavioral alterations, with a particular focus on intestinal necroptosis-associated signaling. In a DSS-induced colitis model, PSE reduced body weight loss, colon shortening, systemic inflammatory cytokine levels, and tissue injury-associated epithelial cell death, while also attenuating colonic necroptosis-associated signaling. Open-field and tail-suspension tests further showed that PSE improved behavioral indices associated with anxiety- and depression-/despair-like responses in DSS-treated mice. Consistently, PSE reduced inflammatory signaling and glial activation in the hippocampus and prefrontal cortex. In vitro, PSE protected intestinal epithelial cells from injury induced by a necroptosis-triggering combination of a Smac mimetic and zVAD-FMK (SZ), accompanied by reduced ROS production and inhibition of RIP1-RIP3-MLKL pathway activation. Fractionation-guided isolation of PSE identified five major constituents, all of which suppressed SZ-induced cell death and necroptosis-associated signaling at non-cytotoxic concentrations. Network-based analysis further identified putative molecular mediators linking PSE constituents to necroptosis-related pathways. Collectively, these findings suggest that PSE attenuates DSS-induced intestinal inflammatory injury and colitis-associated central inflammatory and behavioral alterations through suppression of necroptosis-associated signaling.
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