| Background and Aims:Inflammatory bowel disease(IBD)is chronic,refractory and recurrent intestinal inflammatory diseases.The etiological factors have not been clear yet,but now it regarded as excessive immune response of gut microbiota in genetic susceptibility patients.FP(Faecalibacterium prausnitzii)bacteria is one of the common gut microbiota,and recent studies suggest that it can protect the intestinal mucosa.Although FP and its metabolites can reduce intestinal inflammation response,the specific mechanism has not been recognized.Inflammasomes are intracellular multiprotein complexes which are considered to regulate host defense of microorganisms and to maintain intestinal homeostasis.The immune dysregulation of gut microbiota can lead to IBD and bowel cancer.NLRP3 inflammasomes,which comprise of NLRP3、ASC and caspase-1,play an important role in the pathogenesis of IBD,although the mechanism is still unclear.The aims of present study were to investigate the effects and potential mechanisms of Faecalibacterium prausnitzii(FP)on NLRP3 inflammasomes in rats colitis.Methods:40 Sprague Dawley(SD)rats were randomly divided into four groups;(each group of 10 rats),which named as normal control group,colitis model control group,F.prausnitzii group and supernatant group,respectively.After keeping the rats off food for 24 hours but with free access to water,Normal control group treated with saline solution(2m L/kg)and the same volume anhydrous ethanol to clyster.The rest three models rats of experimental colitis were established by enema with 2,4,6-trinitrobenzenesulfonic acid(TNBS)(100mg/kg TNBS + the same volume anhydrous ethanol).And then the normal control group and colitis model control group were administered intragastrically with PBS buffer,F.prausnitzii group with live F.prausnitzii and supernatant group with the supernatant of F.prausnitzii for 1-7 days.Then disease activity index(DAI)was evaluated by recording the mental condition,diet,stool property and weight changes of rats.The length of the colon,the score of macroscopic injury and histological change of colon were observed.The expression of intestinal NLRP3,ASC and caspase-1 were detected by immunohistochemistry.Results:There was a significant lower in DAI and histological damage in groups which were administrated by gavage of either FP(5.60±0.47)or supernatant(5.14±0.50)than that in colitis model group(8.70±0.35,P<0.05).Compared with normal group(13.10±0.66cm),the lengths of colon of colitis model group,FP group(12.35±0.67 cm)and the supernatant group(12.60±0.57 cm)were shortened(colitis and FP group P values < 0.05).Compared with the colitis model group(11.65 ± 0.67 cm),the lengths of colon of the rest three groups were extended and the differences were statistically significant(P < 0.05).The Neurath scores in normal control group,the colitis model group,FP group and supernatant group were 0.70±0.67,3.10±0.88,2.30±0.95 and 2.50±0.97,respectively.The scores of the other three groups were significantly increased compared with the normal group.Whereas,only the scores of the normal group and supernatant group were significantly lower than the colitis model group(P < 0.05).The statistical trends of NLAR3 and caspase-1 were similar in colon tissue.Compared with the normal group(0.80±0.63,1.00±0.67,the expression of NLRP3 and caspase-1 in other three groups was increased,but was more obvious in colitis rat intestinal tissue(5.10±0.88,4.80±1.23)(P < 0.05).However,the expressions of NLRP3 and caspase-1 were no obvious differences in the supernatant group(2.50±0.97,2.90±1.79)and FP group(3.10±0.99,3.60±1.26.The expressions of ASC protein were increased in colitis group(4.90 ±1.19),supernatant group(3.30 ± 1.70)and FP group(4.30±1.34)compared to the normal group(0.60± 0.69).Conclusions:FP and its supernatant had a potential promoting effect on repairing intestinal mucosa in rat with colitis induced by TNBS and could inhibit the expression of NLRP3 inflammasome in intestinal tissue.The treatment effect of FP and its supernatant in intestinal inflammation might be related to inhibiting the overexpression of NLRP3 inflammasome. |
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