| Background and aimsIn the past, the incidence of Ulcerative colitis (UC) was not high inChina, and majority of the patients belong to mild or not typical cases. Inrecent years, with the improvement of living level, the incidence rate ofUC was increased year by year. Colon and rectum in which have most gutbacteria are the most places that UC is present, and the changes of eatinghabits are closely related to sorts and quantities of gut bacteria. Somestudies speculated that the latent etiology of UC is related to some sorts ofgut bacteria. The most common drugs for UC treatment includedacetylsalicylic acid, corticosteroids, and immunosuppressive agents, butthese drugs have some disadvantages such as more side-effects and clinicalrelapse after no maintenance treatment. Recently, some studies confirmedthat probiotics (beneficial bacterial species) have some effects to treatmentof UC, and they also have little side-effects, but the mechanism of thistreatment is unclear.Tumor necrosis factor (TNF)-αis the most important proinflammtorycytokine and immunoregulation factor. Some studies confirmed thatTNF-αcan be an index which can observe the activity of UC.Cyclooxygenase (COX) is the rate-limiting enzyme in the productionof prostanoids from arachidonic acid. There are two isoforms of COX; COX-1 is constitutive form, which regulates gastrointestinal homeostasisthrough the synthesis of prostaglandins (PGs), and that is "housekeeping".COX-2 is the inducible form, and in general, majority of cells in humanbody have no COX-2 expression, and the expression of COX-2 can beinduced by various stimuli such as cytokines and carcinogenesis.The aim of this study was to investigate the therapeutic effects ofprobiotics (Lactobacillus and Bifidobacteria) to Dextran Sulfate Sodium(DSS)-induced UC mouse model, and detect the levels of TNF-αandCOX-2 expression in colorectal mucosa, and further elucidate thepathogenesis of UC. It will provide a new way for UC treatment.MethothsDSS-induced UC BALB/c mouse model was used in the present study.A total of 60 mice were divided into 6 groups. They included Blank controlgroup, DSS-induced mouse model group, Saline group, SASP treatmentgroup, Lactobacillus treatment group and Bifidobacteria treatmentgroup(n=10/group). All of the mice except Blank control group were fedwith 5%DSS. Before 2 days, each group of the mice was given Saline,SASP, Lactobacillus and Bifidobacteria by clysis, respectively. After 8days, the mice of each group were sacrificed, and colonic specimens wereembedded in paraffin and cut into sections which were stained withhematoxylin-eosin, and the conditions of mice were observed, andhistological injury score in colorectal mucosa and pathological examination were detected, and the levels of TNF-αand COX-2expression in colorectal mucosa were determined byImmunohistochemical staining.Results1. The general conditions of mice were much better, and the weight ofmice and blood of defecate were significantly reduced in Lactobacillustreatment group, Bifidobacteria treatment group and SASP group,compared with that in the DSS-induced group and Saline group of mice (P＜0.05).2. The histological injury score in colorectal mucosa was significantlyreduced in Lactobacillus treatment group and Bifidobacteria treatmentgroup, compared with that in the DSS-induced group and Saline group ofmice (P＜0.05), but there was no significance, compared with that in theSASP treatment group (P＞0.05).3. The levels of TNF-αand COX-2 expression in colorectal mucosawere significantly decreased in Lactobacillus treatment group andBifidobacteria treatment group, compared with that in the DSS-inducedgroup and Saline group of mice (P＜0.05), but there was no significance,compared with that in the SASP treatment group (P＞0.05).Conclusions1. Both Lactobacillus and Bifidobacteria are effective to treatment ofDSS-induced UC in mice. 2. Lactobacillus and Bifidobacteria have the roles of treatmem toDSS-induced UC of mice, probably mainly via inhibition of TNF-αandCOX-2 expression in colorectal mucosa.
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