茯苓新酸A通过调节AMPK/mTOR介导的自噬来减轻葡聚糖硫酸钠诱导的小鼠结肠炎

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Abstract：ObjectiveToinvestigatethe mechanismofporicoicacidA（PAA）forallviatingdextransulfate sodium （DSS）- inducedcolitisinmice.MethodsEighteenC57BL/6micewererandomlydividedintocontrolgroup，DS-inducedcolitis model group， and PAA intervention （10mg/kg） group. The changes in body weight， colon length， disease activity index （DAI）， andhistopatolgialoofteweevaaedIudo2elldelngsipss claudin-1--deeedi analyzete mechanisms underlying theameliorating efectofPAAon DS-induced colitis.Results Inthe mouse modelsof DSS-inducedcolitis，AAsignificantlyamelioratedDinducedweightloss，olonsorteningandelevationofDAscor while reducing colonic IL-1β and TNF- α levels. HE staining showed that PAA obviously alleviated colonic crypt damage， reducedinflammatorycellinfiltration，andloweredhistopathological scoresofthecolon.AB-PASstainingrevealed significantlyincreased gobletcellcountsinPAA-treatedmicecomparedtothoseinSgroup.InDSS-inducedCaco-2cels PAAtreatmenteffectivelyinhibitedDS-induceddownregulationofthetightjunctionproteins，reducedBaxandcleaved caspase-esssdss-/dss suggested thatPAA targeted the AMPK/mTOR pathway to activate autophagy and suppresscellapoptosis.Conclusion PAA protectsintestinalbarierfunctionandalleviates DSS-inducedcolitisinmicebyativatingAMPK/mTOR-mediatedautophagy and inhibiting intestinal epithelial cell apoptosis.

teywords： inflammatorybowel disease; poricoicacidA;autophagy; apoptosis; intestinal barrie

炎症性肠病（IBD）是一种以慢性肠道炎症和屏障破坏为特征的疾病，其发病与肠上皮细胞自噬功能受损和凋亡过度密切相关[1-3]。（剩余20168字）