Salidroside mitigates experimental colitis through cyclic adenosine monophosphate pathway activation and suppression of enteric glial cell responses

Figure 9 Schematic representation of the therapeutic mechanism of salidroside in dextran sulfate sodium salt-induced colitis in mice. Salidroside treatment mitigates colitis and restores intestinal mucosal barrier integrity, primarily by activating the cyclic adenosine monophosphate/protein kinase A/cyclic adenosine monophosphate-response element binding protein signaling pathway. This activation inhibits enteric glial cells activation, limits proinflammatory cytokine release, and enhances glial cell line-derived neurotrophic factor secretion. Ultimately, these effects attenuate intestinal inflammation, preserve barrier function, and reduce colonic injury. ZO-1: Zonula occludens-1; cAMP: Cyclic adenosine monophosphate; GFAP: Glial fibrillary acidic protein; GDNF: Glial cell line-derived neurotrophic factor; EGC: Enteric glial cell; IL: Interleukin; TNF: Tumor necrosis factor; NF-κB: Nuclear factor kappa-B; DSS: Dextran sulfate sodium salt; PKA: Protein kinase A.