[Effect of Tripterygium wilfordii polycoride upon inflammation and TLR4/MyD88 signaling pathway in ulcerative colitis rats model].
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To observe the effect of Tripterygium wilfordii polycoride (TWP) on ulcerative colitis (UC), and its intervention effect on toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway, thus to investigate its possible mechanism.Trinitrobenzene sulfonic acid (TNBS)/ethanol enema method was used to set up the UC rat model. With random number table, 90 male Wistar rats were divided into normal control group, model group, TWP low, medium and high dose group (3, 6, 12 mg/kg, respectively) and azathioprine (AZA) group (6 mg/kg), with 15 rates in each group. Four days after enema, rates in each group were given corresponding drug lavage for 14 consecutive days. Disease activity index (DAI), colon gross morphological damage and histological grading of each group were observed. Using Western blot and reverse transcription (RT)-PCR method, the TLR4/MyD88 signaling pathway-related proteins in UC rat intestinal tissue were detected, namely TLR4, MyD88, tumor necrosis factor receptor related factor 6 (TRAF-6), nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β).The DAI, colon gross morphological damage, and histological grading of the model group were significantly higher than that of the normal control group (all P<0.01), indicating successful establishment of UC model. The DAI, colon gross morphological damage and histological grading of the TWP high dose group were lower than those of the model group (0.87±0.25 vs 1.60±0.76, 3.93±1.94 vs 5.40±2.21, 5.45±2.73 vs 13.27±3.50, P<0.05). Compared with the normal control group, the mRNA and protein expressions of TLR4, MyD88, TRAF-6, NF-κB, TNF-α, and IL-1β in the model group rats were significantly increased (all P<0.01); which were significantly decreased in the TWP high dose group compared with model group rats (mRNA: 2.166±0.475 vs 5.647±0.275, 1.295±0.087 vs 3.774±0.418, 1.125±0.188 vs 2.535±0.320, 1.201±0.152 vs 2.082±0.077, 1.525±0.218 vs 3.094±0.022, 1.797±0.257 vs 17.152±0.145; protein: 0.252±0.010 vs 0.277±0.008, 0.172±0.002 vs 0.213±0.005, 0.233±0.006 vs 0.248±0.003, 0.099±0.003 vs 0.122±0.007, 0.238±0.002 vs 0.252±0.005, 0.235±0.003 vs 0.245±0.006, all P<0.05), also decreased in the AZA group (all P<0.01); and there were no significant differences between the TWP high dose group and the AZA group (all P>0.05).TWP can alleviate intestinal inflammation, promote healing of mucosa, showing a therapeutic effect for UC. One of its mechanisms may be through inhibiting the expression of TLR4, affecting the expression of TRAF-6, which is downstream to MyD66 signaling pathway, thus to suppress the activation of NF-κB and reduce the release of inflammatory factor such as TNF-α and IL-1β.Keywords:
Tripterygium wilfordii
Enema
Tripterygium
In a double-blind controlled therapeutic trial, retention enemas of N-acetyl-5-aminosalicylic acid (Ac-5-ASA) were compared with dummy enemas in the treatment of active ulcerative colitis. Forty patients were studied, each patient taking one test enema twice a day for 2 weeks. Seventeen of the patients had a mild clinical attack of the disease; the 23 others had sigmoidoscopic evidence of active inflammation although they were in clinical remission. Histological and sigmoidoscopic improvement were significantly commoner in the patients receiving the active treatment than in those taking the dummy preparation. Pronounced histological improvement was only seen in patients taking the Ac-5-ASA enemas. In those patients who had clinical attacks of ulcerative colitis at the start of the study, symptomatic improvement was commoner in the group treated with Ac-5-ASA enemas than in those who received placebo therapy. Ac-5-ASA resembles 5-aminosalicylic acid in its effect on the inflamed mucosa in ulcerative colitis. Further studies into other substituted salicylates may lead to the development of an effective oral agent that does not carry the side effects associated with the sulphapyridine moiety of sulphasalazine.
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Aminosalicylic acid
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Mesalazine
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Objective To observe the combined oral mesalazine enema for ulcerative colitis.Methods Totally 240 patients with mild to moderate ulcerative colitis were randomly divided into two groups:treatment group,120 patients to oral mesalazine,1.0g/time,3 times/d,while giving the mesalamine enema(Sa Fu enema,4g/60ml,when diluted with 100ml) 4g/100ml,1 times/night,retention enema,8 weeks as a course;The control group of 120 patients to oral sulfasalazine tablets(Alicylazosulfapyridine,SASP) 1.0g,4 times/d.Treatment for 8 weeks.Results After 8 weeks,the treatment group efficiency and total efficiency is better than the control group,the difference was statistically significant(P0.05);the incidence of adverse reactions of both groups,the treatment group occurred in 13 cases,incidence 10.8%,in the control group of 68 patients,the incidence of 56.7%,treatment group was significantly lower than the control group,the difference was statistically significant(P0.05) .Conclusions Mesalazine has good clinical efficacy in treatment of ulcerative colitis,and less adverse reactions.
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BACKGROUND: The efficacy of mesalazine enemas depends on intraluminal concentration of the drug and is therefore limited by the enema distribution in the colon. Active ulcerative colitis changes colon motility and this leads to uncertainty about enema spread. AIM: To assess the influence of disease activity on enema distribution, we conducted a physician‐blinded, longitudinal study of the retrograde spread of three mesalazine enemas. METHODS: Thirty‐one patients with mild to moderate ulcerative colitis were subdivided into three groups, and treated with 2 g mesalazine in 30 mL (group I, n = 10), 4 g mesalazine in 60 mL (group II, n = 12) or 1 g mesalazine in 100 mL (group III, n = 9). All patients received oral mesalazine 500 mg t.d.s. Enemas were labelled by adding 10 MBq (99mTc)technetium‐sulphur colloid. Anterior scintigraphic images were taken at the start of the study and after 12 weeks of therapy; retrograde spread was assessed by calculating the percentage of the enema in each colonic segment. RESULTS: The activity score of ulcerative colitis diminished significantly after 12 weeks of treatment, but five patients dropped out of the study. At the start of treatment enema activity in group I was mainly concentrated in the sigmoid (99%); in group II activity was found in the rectum (9%), the sigmoid (61%) and the descending colon (15%); in group III activity was distributed between the sigmoid (66%) and descending colon (25%). The colonic distribution of mesalazine enemas was not influenced by disease activity. CONCLUSION: Volume, but not disease activity, is the important determinant of retrograde colonic spread of mesalazine enemas in ulcerative colitis.
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Objective To estabilish rat ulcerative colitis model and observe abnormal NO,MDA,SOD in colon constitution Methods A total of 30 Wister rats which were divided into 3 groups:nomal control;experiment;treatment,which in latter two groups were respectively received saline enemas,SASP(80mg/kg/d)enemas 1ml daily after distal colitis was induced by 8% acetic acid enemas was studed by histopatholog and biochemistry,respectively Results NO(518 7±45 3μmol/g)、MDA(30 6±2 18μmol/g)in experiment group was significantly increased than that in control group(196 5±29 1μmol/g,6 82±0 81μmol/g,P0 01) and treatment group(298 2±27 5μmol/g,14 79±1 92nmol/g,P0 01) But SOD(11 06±1 82u/g)in experiment group was significantly lower than that in control group(22 2±1 62u/g,P0 01)and treatment group(17 7±1 76u/g,P0 01) The damage score(3 89±0 78) in experiment group was notably higher than that in treatment group There were also significant difference between treatment group and control group(P0 01) Concolusions To reduce free radical which involved in the pathological process of the disease can provid a new pahway for therapy ulcerative colitis
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