Ulcerative Colitis: Bai AP

Bai AP, Ouyang Q, Hu RW. · Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China. · J Dig Dis. · Pubmed #17970875 No free full text.

Abstract: OBJECTIVE: Since the etiology and the pathogenesis of inflammatory bowel disease (IBD) are still not well known, research on IBD often focuses on these topics. Investigative science papers about IBD in Chinese medical journals from 1989 to 2003 were viewed to understand the progress of basic IBD research in China. MATERIALS AND METHODS: The basic science investigative papers about IBD from 1989 to 2003 in Chinese periodicals (VIP and CMCC) were reviewed and analyzed; the key words used were as follows: inflammatory bowel disease, ulcerative colitis, Crohn's disease, basic science investigation, and literature review. RESULTS: There were 3454 articles about IBD published in Chinese medical journals from 1989 to 2003, and during these 15 years, 508 papers focused on basic scientific investigations. There were 463 papers investigating the pathogenesis of IBD, 287 papers on immunological mechanisms, and 176 papers about other mechanisms. There were 142 papers investigating the mechanisms of Chinese traditional medicine on IBD from 1989 to 2003, which included 117 papers related to animal experiments and 25 papers related to clinical studies. CONCLUSIONS: There have been relatively few investigative scientific papers on IBD published in Chinese medical journals. However, the study of IBD has been emphasized in China. Research on the immunological mechanisms of IBD has been predominant. Furthermore, a large number of the research papers were about the mechanisms and effects of Chinese traditional medicine on IBD.

Bai AP, Ouyang Q, Xiao XR, Li SF. · Department of Gastroenterology,Westchina Hospital, Sichuan University, Chengdu, China. · Int J Clin Pract. · Pubmed #16494642 No free full text.

Abstract: Enteric microflora of ulcerative colitis patients becomes aberrant. The abnormal interaction between microflora and intestinal mucosal immune system leads the mucosal inflammation. Probiotic administration may recover the commensal microflora and normalise the host-microbial interaction. In this experiment, we cocultured colonic biopsies from active ulcerative colitis patients with bifidobacterium to investigate the modulation effect of probiotics on inflamed colonic tissues and its possible mechanism. Colonic biopsies from active ulcerative colitis were cocultured for 24 h with Bifidobacterium longum. Tumour necrosis factor (TNF)-alpha and interleukin (IL)-8 in supernatants were measured using enzyme-linked immunosorbent assays, the biopsies were fixed using paraffin and the expression of NF-kappaB P65 of tissues was studied using immunohistochemical staining. The concentrations of TNF-alpha and IL-8 in supernatants of tissues cocultured with probiotics were lower than those cultured alone. The number of lamina propria mononuclear cells (LPMC) with nuclear factor-kappa B (NF-kappaB) P65 positive in cocultured tissues was also decreased. When cocultured with inflamed tissues of active ulcerative colitis, probiotics could inhibit NF-kappaB activation in LPMC and down-regulate inflammatory cytokine secretion from inflamed tissues of active ulcerative colitis.

Bai AP, Ouyang Q, Hu RW. · Department of Gastroenterology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou City 510080, China. · Dig Dis Sci. · Pubmed #16110831 No free full text.

Abstract: The present study aimed to investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor (TNF)-alpha expression in inflammed mucosa of ulcerative colitis and its possible mechanism. Colonic biopsies from ulcerative colitis were treated with 0, 1, 5, and 10 microM DATS for 24 hr. Lactate dehydrogenase (LDH) activities and concentrations of TNF-alpha in supernatants were measured. mRNA expressions of TNF-alpha in biopsies were analyzed by RT-PCR. The expression of NF-kappaB P65 in tissues was studied by immunohistochemistry. Concentrations of TNF-alpha in supernatants of biopsies treated with 5 and 10 microM DATS were lower than those of untreated biopsies. There were fewer lamina propria mononuclear cells whose NF-kappaB P65 expression in nuclei was positive, and less mRNA expression of TNF-alpha in biopsies treated with 10 microM DATS than in untreated biopsies. There were no differences in LDH activities in supernatants between tissues treated with DATS and untreated tissues. DATS could downregulate TNF-alpha production and inhibit NF-kappaB activation in lamina propria mononuclear cells of inflammed mucosa, without any effect on the viability of colonic tissue cells.