泄浊解毒方通过调节Th17/Treg免疫平衡改善大鼠溃疡性结肠炎

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Abstract：ObjectiveToexplorethemechanismof XiezhuoJieduRecipe（XZJD）forimprovingulcerativecolitis（UC）.Methods SDrat modelsof UC were randomized into5 groups （n=10）fordaily gavage withsaline，mesalamine，orlow-，medium- or high-doseXZJDfor14days，with10normalrats withsaline gavageas thecontrolgroup.Pathological changesinthecolonof theratswereoseedusingHEstaingandsumIL-6IL-10ndIL-17evelsandteirexpresionsintecolotsee determined with ELISAand immunohistochemistry. The expressions ofocludin and ZO-1and percentages of T17and Treg cellsintecolontisuesweredetectedusing immunofluorescencestainingandflowcytometry;themRNAandprotein expressions of ROR γt and Foxp3 were detected with RT-PCR and Western bloting. Results The rat models of UC showed obviouscolocolgeiieyelilioee-6d-elsdod level inboththeserumandcolonictissues，educedexpressionlevelsofoccluinand ZO-1，increasedTh17ndlowedTreg cell percentages，reasedORytmNAndproteinexpessons，andducedoxp3mAndproteinexpressosthe colonictissue.TreatmentwithXZJDsignificantlyalleviatedinflammatoryresponseinthecolonicmucosaandefectively reversedtegsinI67nd-elseeiosofiadZO-1eagsof7ndTd theexpressionsofRORytandFoxp3inthecolonictissuesofUCrats.ConclusionXZJDcanaleviatepathologiesinthecolonic mucosa in UC rats possibly by regulating Th17/Treg immunebalance.

Keywords：Xiezhuo Jiedu Recipe;ulcerativecolitis;intestinalbarrier;Th17/Treg immunebalance

溃疡性结肠炎（UC）是以慢性炎症反应和肠道黏膜上皮损伤为特征的慢性非特异性炎症性疾病，病变常从直肠黏膜开始向近端发展[2.3]。（剩余17048字）