The Modulatory Effect of Dietary Apostichopus japonicus on Mice with Ulcerative Colitis Induced by Trinitrobenzene Sulfonic Acid

Sea cucumber is a food with nutritional benefits distributing mainly in Asia, and Apostichopus japonicus (A. japonicus) is a kind of sea cucumber whose quality is better than any others. However, different processing methods make various effect on its quality. In this study, we evaluated the protection effect of A. japonicus with different processing methods on mice with ulcerative colitis induced by trinitrobenzene sulfonic acid (TNBS), especially on the intestinal microflora. The expression of IFN-γ/IL-4 and IL-1β in gut, and intestinal microbiota were discussed. The results revealed that three different processing methods of A. japonicus could decrease the expression of inflammatory cytokines, except for the expression of IFN-γ/IL-4 treated with enzymatic, and dried A. japonicus was the most efficient. A. japonicus could change the microbiotic imblance relatively back to normal in terms of bacterial diversity and composition, meanwhile increase the abundance of Bifidobacteria, Lactobacillus and Clostridium leptum. The elements of protein, polysaccharide in dried, instant, enzymatic A. japonicus are 73.09%, 65.06%, 57.42% and 6.72%, 5.46%, 5.45% respectively. This study indicated that A. japonicus have a good improving effect on ulcerative colitis, especially on the microbiome, and processing methods had an effect on alleviation of ulcerative colitis, which might be associated with content of protein and polysaccharide.

Effect of Baicalin on TNBS-Induced Colonic Inflammatory Injury in Rats

Objective: The aim is to observe the protective effect of baicalin on trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis in mice and explore its mechanism. Methods: The mice were divided into 4 groups: ethanol control group, TNBS model group, baicalin low-dose group and baicalin high-dose group. The model of experimental colitis in mice was induced by TNBS enema. After 2 hours of TNBS enema, baicalin was given by gavage, QD × 7D. The animals were sacrificed on the 8th day to observe the extent of colonic mucosal damage, and the Peroxidase activity, Malondialdehyde (MDA) and glutathione (GSH) contents were measured. Results: Compared with the TNBS model group, the body weight, gross injury score and histological changes were significantly improved;MPO enzyme activity and MDA content were significantly decreased in the low and high-dose baicalin groups;and the content of glutathione increased. Conclusion: Baicalin can alleviate TNBS-induced colitis in mice, and the mechanism is related to the antioxidation of baicalin.

Anti-inflammatory efficiency of levobupivacaine in an experimental colitis model

AIM:To investigate the efficiency of levobupivacaine in treating experimentally induced colitis in rats.METHODS:Colitis was induced by trinitrobenzene sulfonic acid and ethanol in 30 rats under general anesthesia,and 10 rats were used as a sham group.Subsequent to induction of colitis,rats were divided into three groups;budesonide group received 0.1 mg/kg budesonide,levobupivacaine group received 10 mg/kg levobupivacaine and saline group received 1 mL saline solution via rectal route for 7 d.In the sham group,only routine rectal catheterization was performed without use of any material.At the end of 7 d,laparotomy and total colectomy were performed for histopathological ex-amination in all rats and blood samples were drawn for measurement of tumor necrosis factor(TNF)-αand interleukin(IL)-6 following cardiac puncture.Macroscopic and microscopic evaluations of the specimens were performed by a pathologist blinded to group assignment of the rats.RESULTS:Weight loss(P=0.016)and macroscopic examination scores(P=0.001)were significantly higher in saline group than others.Histopathological scoring was comparable between all colitis groups(P=0.350).There was no significant difference in TNF-αlevels and IL-6 levels(P=0.150).CONCLUSION:The significant improvement in macroscopic scores suggests that levobupivacaine may have topical anti-inflammatory effects in an experimental colitis model;however,this finding was not supported by microscopic findings.

Role of β2-Adrenoceptor-β-Arrestin2-Nuclear Factor- k B Signal Transduction Pathway and Intervention Effects of Oxymatrine in Ulcerative Colitis

Objective： To investigate the β2-adrenoceptor （ β 2AR）-β-arrestin2-nuclear factor- K B （NF- κ B） signal transduction pathway and the intervention effects of oxymatrine in a rat model of ulcerative colitis. Methods： Forty SD rats were randomly divided into four groups, which included the normal control group, the model group, the mesalazine group and the oxymatrine treatment group, with 10 rats per group. Experimental colitis induced with trinitrobenzene sulfonic acid （TNBS） was established in each group except the normal control group, The rats in the oxymatrine treatment group were treated with intramuscular injection of oxymatrine 63 mg/（kg.d） for 15 days and the rats in the mesalazine group were treated with mesalazine solution 0.5 g/（kg.d） by gastric lavage for 15 days. The rats in the normal control group and model group were treated with 3 mL water by gastric lavage for 15 days. Diarrhea and bloody stool were carefully observed. Histological changes in colonic tissue were examined on day 7 in 2 rats per group that were randomly selected. The expression of β 2AR, β -arrestin2 and NF- κ B p65 in colon tissue and spleen lymphocytes were detected with immunohistochemistry and Western immunoblotting techniques on day 16 after fasting for 24 h. Six rats died of lavage with 2 each in the normal control, the model group and the mesalazine group; and were not included in the analysis. Results： The rats in the model group suffered from looser stool and bloody purulent stool after modeling. But in the oxymatrine and mesalazine groups, looser stool and bloody purulent stool reduced after treatment. And the colonic wall in the model group was thickened and the colon length shortened. The colon mucosa was congested in multiple areas with edema, erosion, superficial or linear ulcer and scar formation, while the intestinal mucosa injury reduced in the mesalazine and oxymatrine groups （P〈0.01）. In colonic mucosa and in spleen lymphocytes, compared with the normal control group, the expression of NF- κ Bp65 were significantly increased （P〈0.01） in the model group while the expressions of β 2AR and β-arrestin2 were significantly decreased （P〈0.01）. Compared with the model group, the expression of NF- κ Bp65 was significantly decreased in the mesalazine group （P〈0.01） and oxymatrine treatment group （P〈0.01） while the expressions of β 2AR and β -arrestin2 were significantly increased （P〈0.01）. There were no statistically significant differences in the expression of β 2AR, β -arrestin2 and NF- κ Bp65 between the mesalazine group and oxymatrine group （P〉0.05）. Conclusions： The β 2AR- β -arrestin2-NF- κ B signal transduction pathway participated in the pathologic course of ulcerative colitis. Oxymatrine attenuated ulcerative colitis through regulating the β 2AR- β -arrestin2-NF- κB signal transduction pathway.

Effect of homocysteine on intestinal permeability in rats with experimental colitis,and its mechanism

Objective:To investigate the effect of homocysteine(Hcy)on intestinal permeability in rats with TNBS/ethanol-induced colitis and elucidate its mechanism.Methods:Sprague-Dawley rats were divided into four groups:normal,normal+Hcy injection,TNBS model,and TNBS model+Hcy injection.Experimental colitis was induced by trinitrobenzene sulfonic acid(TNBS)in 50%ethanol;rats were injected subcutaneously with Hcy from the first day after the induction of experimental colitis on 30 consecutive days.To determine the severity of colitis,the disease activity index(DAI)was evaluated;colon tissues were collected for the detection of the activity of myeloperoxidase(MPO)and the contents of MDA,IL-1β,IL-6,TNF-α,MMP-2,and MMP-9.Intestinal epithelial permeability was assessed with Evans blue(EB)dye.The levels of Hcy in plasma and colon mucosa were measured by high-performance liquid chromatography-fluorescence detection(HPLC-FD).Results:Compared with the normal group,the DAI scoring and MPO activity,contents of MDA,IL-1β,IL-6,TNF-α,MMP-2,and MMP-9in the colon and EB in the small intestine were significantly increased in the TNBS group(P<0.01).Compared with the TNBS model group,the DAI scoring,plasma and colonic mucosa Hcy levels,MPO activity and contents of MDA,IL-1β,IL-6,TNF-α,MMP-2,and MMP-9 in colon and EB in small intestine were significantly increased in the TNBS-induced colitis rats with simultaneous Hcy injection(P<0.01).Conclusion:Hcy can increase intestinal permeability and aggravate inflammatory damage in rats with TNBS-induced colitis,the underlying mechanisms of which may be attributed to its effects of promoting the expression of MMP-2 and MMP-9,leading to injury of the intestinal barrier.