Abstract:Objective: To investigate the protective effect of polysaccharide D from Ophiopogon japonicus (MCD) on inflammatory bowel disease (IBD) in rats and its potential mechanism. Methods: Male SD rats were randomly divided into 5 groups: control group, model group, MCD low-dose group (50 mg/kg·d), MCD high-dose group (100 mg/kg·d), and MCD+H-89 group (100 mg/kg·d MCD+5 mg/kg·d H-89). The model group was induced by 2,4-dinitrochlorobenzene (DNCB) sensitization and repeated intracolonic administration of DSS. The treatment groups were given MCD or MCD+H-89 for 28 days. Body weight, colon length, serum IL-10, cAMP levels, proportions of Treg cells in peripheral blood, expressions of Bcl-2, p-PKA/PKA, p-CREB/CREB proteins in colon tissues, serum IL-17, IL-6, TNF-α levels, proportions of Th17 cells and Th17/Treg ratios in peripheral blood, and Bax protein expression were determined. Results: After treatment, compared with the control group, the model group rats showed significant colon tissue damage, decreased body weight and colon length, decreased serum IL-10 and cAMP levels, decreased proportions of Treg cells in peripheral blood, decreased expressions of Bcl-2, p-PKA/PKA, p-CREB/CREB proteins in colon tissues, increased serum IL-17, IL-6, TNF-α levels, increased proportions of Th17 cells and Th17/Treg ratios in peripheral blood, and increased Bax protein expression (P<0.05). Compared with the model group, the colon tissues of rats in the MCD low-dose and high-dose groups were significantly alleviated, body weight and colon length were increased, serum IL-10 and cAMP levels were increased, proportions of Treg cells in peripheral blood were increased, expressions of Bcl-2, p-PKA/PKA, p-CREB/CREB proteins in colon tissues were increased, serum IL-17, IL-6, TNF-α levels were decreased, proportions of Th17 cells and Th17/Treg ratios in peripheral blood were decreased, and Bax protein expression was decreased (P<0.05). H-89 could partially reverse the therapeutic effect of MCD on IBD rats (P<0.05). Conclusion: MCD can reduce the inflammatory response and colon tissue damage in IBD rats, possibly by activating the cAMP/PKA/CREB signaling pathway.
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