| Background:Ulcerative colitis is a non-specific inflammatory bowel disease, but its etiopathogenisis was not very clear. At present, most scholars believe that the pathogenesis of UC which is the environmental factors affecting the genetic susceptible, with the participation of intestinal microorganisms, which started the damage mechanisms of intestinal mucosal immune response, thus leading to immune response and inflammation. Although the current preparation of Salicylic Acid, glucocorticosteroid, immunosuppressive agents and biological agents targeting on UC treatment which was effective to a certain extent, they have brought disadvantages to patients owing to its side effects, long drug administration and relapse easily after discontinuation. Some researches have shown that intestinal microflora structure of UC patients is changed, it can be significantly improved by giving probiotics to regulate intestinal micro-environment. Therefore, the application of probiotics treatment or adjuvant treatment to UC which has become one of the important topics in the basic and clinical researches. Some studies confirmed that cytokines (such as IL-1β,TNF-a,IL-6,ect.)plays an important role in the incidence and development of ulcerative colitis, they can induce and activate various inflammatory cells, promoting the release of inflammation cytokines, thereby cause the inflammation of intestinal mucosal. The expression of these cytokines has been regulated by nuclear factor NF-kB at the transcription level. Therefore, by inhibiting NF-κB activation, we can reduce the expression of pro-inflammatory cytokines and intestinal mucosal immune response of UC patients.In recent years, studies have shown that apoptosis may also be an important mechanism in the pathogenesis of UC. Bcl-2 family which is a core member of apoptosis gene families plays an important role in apoptotic process. Bcl-2 protein which is usually located in the outer membrane of cell mitochondria and endoplasmic reticulum, controlling the release of pro-apoptotic factors, which can inhibit apoptotic; while Bax protein can induce the release of cytochrome C and other pro-apoptotic factors, activating of downstream signaling pathways, initiating cell apoptosis.Therefore, Bcl-2 and Bax protein ratio plays an important role in maintaining homeostasis of cell physiological differentiation and numbers. Objectives:This study was to investigate the treatment of Bnfillus licheniformis on acute ulcerative colitis in mice, and observe the expression level of NF-κB,Bcl-2 and Bax in colorectal mucosa, further discussed the possible mechanism of probiotic treatment of UC. This will provides a new theory for probiotic treatment of adjuvant treatment of UC.Methods:1. Dextran sulfate sodium(DSS) induced BABL/c mouse model of acute ulcerative colitis was used in this study.64 BABL/c mouse were randomly divided into 8 groups, every group 8 mouse, that:Blank control group. DSS-induced mouse model group. CMC-Na treatment group,SASP treatment group. Bnfillus licheniformis high-dose combined SASP treatment group. Bnfillus licheniformis high-dose treatment group,Bnfillus licheniformis low-dose combined SASP treatment group and Bnfillus licheniformis low-dose treatment group. All of the mice except Blank control group were fed with 4%DSS solution drinking freely 7 days, and at the same time were administrated in modeling the first day. In modeling the 8th day,4% DSS drinking water was replaced by the distilled water, and to continue drug treatment for 7 days.2. In modeling 15th day, all the mice were sacrificed. Colonic specimens were embedded in paraffin wax and cutted into sections which were stained with hematoxylin eosin. The general situation of mice were observed, and gross injury score in colorectal mucosa and histopathological changes were detected. The expression level of NF-κB, Bcl-2 and Bax in mouse colorectal mucosa were also determined by immunohistochemistry method, and explore the possible mechanism with the expression level of NF-κB, Bcl-2 and Bax and Bnfillus licheniformis treatment of UC.Results:1. Compared with DSS-induced mouse model group and CMC-Na treatment group, general conditions of other treatment groups were better, increased significantly in body weight, blood would be less or no(P<0.05).2 Compared with DSS-induced mouse model group and CMC-Na treatment group, gross injury score in colorectal mucosa and histopathological changes of other treatment groups were decreased significantly, there were distinguished differences(P<0.05); Moreover, with Bnfillus licheniformis high-dose combined SASP treatment group and Bnfillus licheniformis low-dose combined SASP treatment group compared to SASP alone treatment group, the difference is statistically significant(P<0.05); But with Bnfillus licheniformis high-dose treatment group and Bnfillus licheniformis low-dose treatment group compared to SASP alone treatment group, there were no significance(P>0.05).3. Compared with DSS-induced mouse model group and CMC-Na treatment group, the expression level of NF-κB and Bcl-2 of other treatment groups were all decreased significantly, there were distinguished differences(P<0.05); In addition, with Bnfillus licheniformis high-dose combined SASP treatment group and Bnfillus licheniformis low-dose combined SASP treatment group compared to SASP alone treatment group, the difference of the expression level of NF-κB and Bcl-2 is also statistically significant(P<0.05); But with Bnfillus licheniformis high-dose treatment group and Bnfillus licheniformis low-dose treatment group compared to SASP alone treatment group, there were no significant variability (P>0.05). However, the expression level of Bax is opposite to aforesaid factors.Conclusions:1. Bnfillus licheniformis has been therapeutical effect to DSS-induced acute ulcerative colitis in mice, and there was more effective when the administration of it combined with SASP.2. The therapeutical effect of Bnfillus licheniformis to UC is probable by inhibiting the expression of NF-κB and Bcl-2, and up-regulating the expression of Bax in colorectal mucosa.
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