Effect of curcumine in regulating the balance between regulatory T cells/helper T lymphocyte 17 via SOCS3 in inflammatory bowel disease in immature rat / 中华实用儿科临床杂志

ABSTRACT

Objective To determine the therapeutic efficacy of curcumine on inflammatory bowel disease(IBD)and its underlying mechanisms.Methods The rat ulcerative colitis model was developed by using 30 g/L dextran sulfate sodium.Twenty-four young rats were divided into 4 groupsnormal group,model group,curcumin 100 mg/kg group(curcumin 100 group),and curcumin 300 mg/kg group(curcumin 300 group).Curcumin was given through gastric gavage once a day for 7 days.General condition,disease activity index(DAI)and histopathological score(HPS)were evaluated.The proportions of CD4+ CD25+ Foxp3+ regulatory T cells(Treg)and CD4+ IL-17+ helper T lymphocyte 17(Th17)in CD4+ T cells in rats,and spleen cells were calculated by using flow cytometry.Immunohistochemical method was performed to determine the level of SOCS3 in colon tissues.Results After curcumin administered through gastric gavage for 5 days,compared with the DAI in the model group[(7.50±0.32)scores],HPS in the curcumin 100 group[(4.00±1.10)scores] and the curcumin 300 group [(5.00±0.89)scores] significantly reduced,and the difference was significant(F=12.469,P0.05).Compared with the model group[(6.5±1.5)％],the propotion of CD4+ CD25+ Foxp3+ Treg cells in CD4+ T cells in the curcumin 100 group[(9.9±1.0)％],the curcumin 300 group [(9.3±0.7)％] and the normal group[(9.6±1.1)％]was obviously upregulated(F=16.635,P0.05).Compared with the model group[(3.5±1.4)％],the propotion of CD4+ IL-17+ Th17 cells in CD4+ T cells in the curcumin 100 group[(2.0±0.9)％],the curcumin 300 group [(1.2±0.6)％] and the normal group[(2.0±0.9)％] was downregulated(F=5.155,P0.05).There was no obvious difference between the curcumin 100 group and the curcumin 300 group in these indicators respectively(all P>0.05).Conclusions Curcumin probably attenuates IBD severity,reduces inflammation and regulates the balance of Treg/Th17 through the inhibition of SOCS3 expression.