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Review The recent studies on treatment of the damaged intestinal mucosa. 2003
Chen Y, Chen W. · Guangzhou University of Traditional Chinese Medicine, Guangzhou 510224. · J Tradit Chin Med. · Pubmed #14719305 No free full text.
This publication has no abstract.
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Article Is exercise beneficial to the inflammatory bowel diseases? An implication of heat shock proteins. 2009
Chen Y, Noble EG. · School of Kinesiology, Faculty of Health Sciences, University of Western Ontario, London, Ontario, Canada N6A 3K7. · Med Hypotheses. · Pubmed #18829174 No free full text.
Abstract: Inflammatory bowel diseases (IBD) cause the intestines to become inflamed (red and swollen) and typically include Crohn's disease and ulcerative colitis. Heat shock protein (Hsp)70, which exhibits greater expression in the intestines of patients with IBD, may act to protect the intestine against this inflammatory insult. However, most procedures for eliciting this protective response, such as heating and/or pharmacological interventions are non-physiological and can have serious side-effects. Exercise is a biologically relevant means of inducing protective heat shock proteins in the myocardium and other organs but it has yet to be studied in the bowel. We herein hypothesize that (1) exercise will be beneficial in reducing the occurrence of IBD and suppressing intestine inflammatory injuries, (2) exercise will provide protection through induction of anti-inflammatory Hsps. Further studies using both genetically manipulated animal models and animals undergoing exercise are needed to determine the efficacy of exercise and the role of Hsps in inhibiting or treating inflammatory bowel disease.
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Article [Protective effect of epigallocatechin-3-gallate on inflammatory bowel disease: experiment with rat models of induced colitis] 2007
Lin YZ, Chen Y, Song YG. · Institute for Digestive Medicine of Nanfang Hospital, Southern Medical University, Guangzhou, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #18261323 No free full text.
Abstract: OBJECTIVE: To explore the protective effect of epigallocatechin-3-gallate (EGCG) on ulcerative colitis (UC) and mechanism thereof. METHODS: Sixty SD rats underwent enema of trinitrobenzene sulfonic acid (TNBS) to cause UC and then randomly divided into 6 groups: model group, undergoing enema of normal saline (NS) once a day for 2 weeks; positive drug control group, undergoing enema of 5-aminosalicylic acid (ASA), an anti-UC drug; high-dose EGCG group, undergoing enema of 100 mg/kg EGCG; low-dose EGCG group, undergoing 5 enema of 50 mg/kg EGCG; and EGCG pretreatment group, undergoing enema of 100 mg/kg once a day 3 days before the model establishment and then once a day for 2 weeks after the model establishment. Another 12 rats were used as normal controls. Two weeks later the rats were killed. The histological score of the colonic mucosa was evaluated. The cyclooxygenase-2 protein expression in the colonic mucosa was detected by immunohistochemistry and the cyclooxygenase-2 mRNA expression was assessed by semiquantitative reverse-transcription polymerase chain reaction. RESULTS: The histological score of the model group was 6.4 +/- 2.7, significantly higher than that of the normal control group (1.0 +/- 0.7, P < 0.01). The histological scores of the 5-ASA, and 100 mg/kg and 50 mg/kg EGCG groups were 3.4 +/- 1.8, 2.6 +/- 1.5, and 4.0 +/- 2.0 respectively, all significantly lower than that of the model group (all P < 0.05). The histological scores of the EGCG pretreatment group was the lowest (1.2 +/- 0.8), especially compared with the model group (P < 0.01). Cyclooxygenase -2 mRNA was not expressed in the normal control group, was highly expressed in the model group, and the expression levels of the 5-ASA and EGCG groups were all significantly lower than that of the model group (chi(2) = 22.017, P < 0.05). CONCLUSION: Preventing and ameliorating colitis by inhibiting cyclooxygenase-2 activity, EGCG may be a potential medicine in treating inflammatory bowel disease.
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Article A comparison of autonomic function in patients with inflammatory bowel disease and in healthy controls. 2007
Ganguli SC, Kamath MV, Redmond K, Chen Y, Irvine EJ, Collins SM, Tougas G. · Division of Gastroenterology, Department of Medicine, McMaster University, Hamilton, ON, Canada. · Neurogastroenterol Motil. · Pubmed #17931336 No free full text.
Abstract: We evaluated autonomic function, symptoms and psychological parameters in patients with ulcerative colitis (UC), Crohn's disease (CD) and matched controls to assess whether UC patients have greater basal sympathetic autonomic activity. Outpatients with UC (n = 15), CD (n = 13) and healthy controls (n = 28) underwent spectral analysis of heart rate variability to assess cardiac autonomic function, a methacholine challenge to assess cholinergic pulmonary responsiveness, and questionnaires assessing disease severity, anxiety and depression. UC but not CD patients had greater sympathetic activity than controls with increased absolute (6600 vs 5884; P = 0.04) and relative (62.8%vs 54.8%; P = 0.02) low frequency areas. This was not because of increased overall autonomic nervous system (ANS) activation and was independent of disease activity. In UC patients, trait (personality-related) anxiety correlated strongly with disease symptoms (R = 0.84; P < 0.001) and quality of life (R = -0.81; P < 0.001) while situational (state) anxiety did not. In CD patients, ANS measures were similar to controls and disease activity was unrelated to psychological measures. Cholinergic pulmonary responsiveness was normal in both UC and CD patients. UC patients have an increased sympathetic ANS activity which is independent of symptom severity. In these patients symptom severity is strongly associated with measures of personality related (but not current) anxiety.
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Article Induction of experimental acute ulcerative colitis in rats by administration of dextran sulfate sodium at low concentration followed by intracolonic administration of 30% ethanol. free! 2007
Chen Y, Si JM, Liu WL, Cai JT, Du Q, Wang LJ, Gao M. · Department of Gastroenterology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China. · J Zhejiang Univ Sci B. · Pubmed #17726744 links to free full text
Abstract: Several models of experimental ulcerative colitis have been reported previously. However, none of these models showed the optimum characteristics. Although dextran sulfate sodium-induced colitis results in inflammation resembling ulcerative colitis, an obvious obstacle is that dextran sulfate sodium is very expensive. The aim of this study was to develop an inexpensive model of colitis in rats. Sprague-Dawley rats were treated with 2% dextran sulfate sodium in drinking water for 3 d followed by an intracolonic administration of 30% ethanol. The administration of 2% dextran sulfate sodium followed by 30% ethanol induced significant weight loss, diarrhea and hematochezia in rats. Severe ulceration and inflammation of the distal part of rat colon were developed rapidly. Histological examination showed increased infiltration of polymorphonuclear leukocytes, lymphocytes and existence of cryptic abscesses and dysplasia. The model induced by dextran sulfate sodium at lower concentration followed by 30% ethanol is characterized by a clinical course, localization of the lesions and histopathological features similar to human ulcerative colitis and fulfills the criteria set out at the beginning of this study.
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Article Validation of the mainland Chinese version of the Inflammatory Bowel Disease Questionnaire (IBDQ) for ulcerative colitis and Crohn's disease. free! 2007
Ren WH, Lai M, Chen Y, Irvine EJ, Zhou YX. · Department of Nursing, Second Affiliated Hospital, College of Medicine, Zhejiang University, PR China. · Inflamm Bowel Dis. · Pubmed #17309070 links to free full text
Abstract: BACKGROUND: Inflammatory bowel disease affects the quality of a patient's life in many ways, but no validated instrument for measuring disease-specific quality of life in these patients is available for use in Mainland China. The aim of our study was to develop and validate the Mainland Chinese translation of the Inflammatory Bowel Disease Questionnaire for ulcerative colitis (UC) and Crohn's disease (CD) by assessing its construct validity, discriminant ability, reliability, and sensitivity to change. METHODS: We administered a developed Mainland Chinese version of the Inflammatory Bowel Disease Questionnaire (IBDQ). Ninety-two Mainland Chinese patients (52 with UC and 40 with CD) completed the Mainland Chinese version of the IBDQ, the Chinese version of SF-36, and the global scale for general well-being. A subgroup of 71 patients also completed the Mainland Chinese version of the IBDQ and the global scales for general well-being on a second occasion. Clinical activity was assessed by the Walmsley and Harvey-Bradshaw simple indices. RESULTS: The Mainland Chinese IBDQ scores correlated well with the related SF-36 dimensional scores for all 4 domains (r = 0.51-0.82), SF-36 total scores (r = 0.58-0.87), the colitis activity index (r = -0.56-0.74), and the CD activity index (r = -0.64-0.78) as well as with the global scales. The Mainland Chinese IBDQ was able to discriminate between active and inactive disease. Cronbach's alpha was 0.95 in UC and 0.94 in CD. Test-retest reliability was excellent (intraclass correlation coefficient 0.69-0.93) when it was repeated in patients whose clinical activity index was stable. In contrast, there was a significant difference between the baseline and follow-up measurements in patients whose clinical activity index was changed. CONCLUSIONS: The Mainland Chinese IBDQ proved to be a valid, discriminative, and reliable instrument for assessing health-related quality of life in patients with UC and CD in Mainland China.
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Article Inflammatory bowel disease in patients with celiac disease. 2005
Yang A, Chen Y, Scherl E, Neugut AI, Bhagat G, Green PH. · Department of Medicine, Pathology and Herbert Irving Comprehensive Cancer Center, Columbia University College of Physicians and Surgeons, New York, New York, USA. · Inflamm Bowel Dis. · Pubmed #15905699 No free full text.
Abstract: BACKGROUND: Several case reports and series report an association between celiac disease and inflammatory bowel disease (IBD); however, there is no current data assessing this association. We therefore studied the occurrence of these conditions in a cohort of patients with celiac disease seen at a referral center. METHODS: A database of patients with celiac disease seen between 1981 and 2002 was analyzed. Only biopsy-proven adults were included. Patients who had endoscopic and pathologic evidence of IBD were identified, and their pathology was reviewed. Age- and sex-adjusted prevalence rate ratios were determined by comparing results with population-based prevalence data. RESULTS: Among 455 patients with celiac disease, IBD was identified in 10 (5 had ulcerative colitis and 5 had Crohn's disease). This represented an age- and sex-adjusted prevalence rate ratio for ulcerative colitis of 3.56 (95% confidence interval, 1.48-8.56) and for Crohn's disease of 8.49 (95% confidence interval, 3.53-20.42). CONCLUSION: Within our cohort of patients with celiac disease, IBD was significantly more common than in the general population.
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Article [The effects of anti-inflammatory on activation of nuclear factor-kappaB and expression of cell adhesion molecules in patients with ulcerative colitis] 2004
Chen Y, Gan H, Ouyang Q, Xu D, Pan Y, A Z. · Department of Life Sciences, Dali College, Dali 671000, China. · Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. · Pubmed #15553846 No free full text.
Abstract: The purpose of this study is to assess the effects of anti-inflammatory on activation of nuclear factor-kappaB and mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in intestinal mucosal biopsy specimens from patients with ulcerative colitis (UC). A total of 27 cases with UC were investigated. 15 cases received sulfasalazine (SASP) treatment or SASP and glucocorticoid treatment, 12 cases did not receive any medication related with UC. Normal mucosa from 9 colon cancer cases served as control. Ten pieces of intestinal mucosal biopsy specimens were obtained from each patient. The mRNA expression of ICAM-1 and VCAM-1 were determined by reversal transcription-polymerase chain reaction (RT-PCR). The protein levels of ICAM-1 and VCAM-1 were measured by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay (EMSA). The results showed that NF-kappaB DNA binding activity, mRNA and protein expression of ICAM-1 and VCAM-1 were increased significantly in patients with UC, compared with normal control (P<0.05). Glucocorticoids and SASP markedly inhibited NF-kappaB activation and significantly decreased mRNA and protein expression of ICAM-1 and VCAM-1 (P<0.05). Adhesion molecules (ICAM-1 and VCAM-1) gene activation had significant positive correlation with the NF-kappaB DNA binding activity (r=0.8652 P<0.05, r=0.7902, P<0.05, respectively). We concluded that NF-kappaB is a major and essential factor in regulating the expression of adhesion molecules, it plays an important role in the pathogenesis of UC. SASP and glucocorticoids ameliorate UC via inhibition of NF-kappaB activation and reduction of adhesion molecules expression.
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Article [The effects of nuclear factor-kappa B p65 antisense oligonucleotides on expression of proinflammatory cytokines in lamina propria mononuclear cells from patients with ulcerative colitis] 2003
Gan H, Ouyang Q, Chen Y, Liang F. · Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu 610041. · Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. · Pubmed #12856595 No free full text.
Abstract: To investigate if nuclear factor-kappa B (NF-kappa B) p65 antisense oligonucleotides might affect the expression of NF-kappa B p65 and cytokines in lamina propria mononuclear cells(LPMC) from patients with ulcerative colitis (UC). LPMC were isolated from intestinal mucosal biopsy specimens from 3 patients with UC, and cultured with or without NF-kappa B p65 antisense oligonucleotides (5'-GGAACAGTTCGTCCTATGG-3'), missense oligonucleotides (5'-GGAACAGTTCGTCTATGG-3') and dexamethasone. NF-kappa B p65 expression was determined by western blot analysis. The expression of cytokine mRNA was studied by reversal transcription-polymerase chain reaction (RT-PCR). The cytokine levels were measured by enzyme linked immunosorbent assay. The results showed that NF-kappa B p65 antisense oligonucleotides resulted in down-regulation of NF-kappa B p65 expression, blocked the expression of IL-1 beta mRNA and IL-8 mRNA, and strikingly reduced the production of IL-1 beta and IL-8, and these effects were greater than those of dexamethasone in cultured LPMC from patients with UC(P < 0.05). Therefore, the application of NF-kappa B p65 antisense oligonucleotides may serve as a novel molecular approach for the treatment of patients with UC.
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Article [Activation of nuclear factor-kappaB and effects of anti-inflammatory treatment thereon in intestinal mucosa of patients with ulcerative colitis] 2002
Gan H, Ouyang Q, Chen Y, Xia Q. · Department of Gastroenterology, The West China Hospital Sichuang University, Chengdu 610041, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #11953203 No free full text.
Abstract: OBJECTIVE: To investigate the activation and expression of nuclear factor-kappaB (NF-kappaB) and effects of anti-inflammatory treatment on NF-kappaB in the intestinal mucosa of patients with ulcerative colitis (UC). METHODS: Ten pieces of colon mucosal biopsy specimens were obtained from 31 cases with UC, 17 of which received sulphasalazine (SASP) or SASP plus glucocorticoid and 14 of which received no medication. Samples of normal mucosa around the lesion taken from 11 patients with colon cancer were used as controls. NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay. NF-kappaB p65 expression was determined by Western blot analysis and immunohistochemical staining with a NF-kappaB p65 antibody. The type of cells containing activated NF-kappaBp65 was identified by double immunofluorescence confocal laser scanning microscopy. RESULTS: The expression of NF-kappaB p65 and NF-kappaB DNA binding activity were significantly higher in patients with UC than in the control (P < 0.05), and were correlated with the degree of inflammation. The NF-kappaB expression was significantly stronger in the nuclei than in the cytoplasm in patients with UC without pharmacotherapy. The NF-kappaB expression in nuclei was significantly stronger in the group without pharmacotherapy than in the group with pharmacotherapy (P < 0.05). Only a few NF-kappaB p65 positive cells were seen in the controls. NF-kappaBp65 expression was found in all major subsets of mononuclear cells, including macrophages, B lymphocytes, T lymphocytes, and cryptal epithelial cells. CONCLUSION: The increased activation of NF-kappaB and increased expression of NF-kappaB may be involved in the pathogenesis of UC. Glucocorticoids and SASP strongly inhibited NF-kappaB activation and expression. The inhibition of NF-kappaB activation may be a central part of the anti-inflammatory action of glucocorticoids and SASP, which might represent an important pharmacological mechanism in treatment of patients with UC. NF-kappaB will be an important target for cytokine-based therapy of UC.
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