Ulcerative Colitis: Xiang JY

Xiang JY, Wu LG, Huang XL, Zhang M, Pen L, Ouyan Q, Gan HT. · Department of Gastroenterology, West China Hospital, Sichuan University, Sichuan, China. · Am J Surg. · Pubmed #18926515 No free full text.

Abstract: BACKGROUND: Activation of nuclear factor (NF)-kappaB has been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). The purpose of the current study was to investigate the effects of NF-kappaB decoy oligonucleotides (ODNs) on an experimental model of UC. METHODS: NF-kappaB decoy ODNs were administered in experimental colitis induced by dextran sulfate sodium (DSS). The disease activity index (DAI) and histological score were observed. NF-kappaB DNA binding activity was assessed by electrophoretic mobility shift assay (EMSA). The expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) were measured by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). RESULTS: A significant improvement was observed in DAI and histological score in mice with NF-kappaB decoy ODNs, and the increase in NF-kappaB DNA binding activity, myeloperoxidase (MPO) activity, IL-1beta, and TNF-a in mice with DSS-induced colitis was significantly reduced following administration of NF-kappaB decoy ODNs. CONCLUSIONS: The administration of NF-kappaB decoy ODNs leads to an amelioration of DSS-induced colitis, suggesting administration of NF-kappaB decoy ODNs may provide a therapeutic approach for UC.

Zhang DK, Cheng LN, Huang XL, Shi W, Xiang JY, Gan HT. · Department of Geriatric Medicine and Gastroenterology, West China Hospital, Sichuan University, Chengdu, China. · Int J Colorectal Dis. · Pubmed #18685855 No free full text.

Abstract: BACKGROUND: Activation of nuclear factor (NF)-kappaB has been shown to play a critical role in the pathogenesis of ulcerative colitis (UC), and tetrandrine, a bisbenzylisoquinoline alkaloid isolated from the Chinese herb Radix Stephania tetrandra, has been demonstrated to be a potent inhibitor of NF-kappaB activation. The purpose of the study was to investigate effects of tetrandrine on experimental model of UC. MATERIALS AND METHODS: Tetrandrine was administered in experimental colitis induced by dextran sulfate sodium (DSS). The disease activity index (DAI) and histological score were observed. NF-kappaB DNA binding activity was assessed by electrophoretic mobility shift assay. The expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta were measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. RESULTS: A significant improvement was observed in DAI and histological score in mice with tetrandrine, and the increase in NF-kappaB DNA binding activity, myeloperoxidase activity, IL-1beta, and TNF-alpha in mice with DSS-induced colitis was significantly reduced following administration of tetrandrine. CONCLUSION: The administration of tetrandrine leads to an amelioration of DSS-induced colitis, suggesting administration of tetrandrine may provide a therapeutic approach for UC.

Xiang JY, Ouyang Q, Li GD, Xiao NP. · Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China. · World J Gastroenterol. · Pubmed #18176961 links to  free full text

Abstract: AIM: To investigate possibility and clinical application of fecal calprotectin in determining disease activity of ulcerative colitis (UC). METHODS: The enzyme-linked immunosorbent assay (ELISA) was used to measure the concentrations of calprotectin in feces obtained from 66 patients with UC and 20 controls. C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), acid glycoprotein (AGP) were also measured and were compared with calprotectin in determining disease activity of UC. The disease activity of UC was also determined by the Sutherland criteria. RESULTS: The fecal calprotectin concentration in the patients with active UC was significantly higher than that in the inactive UC and in the controls (402.16 +/- 48.0 microg/g vs 35.93 +/- 3.39 microg/g, 11.5 +/- 3.42 microg/g, P < 0.01). The fecal calprotectin concentration in the inactive UC group was significantly higher than that in the control group (P < 0.05). A significant difference was also found in the patients with active UC of mild, moderate and severe degrees. The area under the curve of the receiver operating characteristics (AUCROC) was 0.975, 0.740, 0.692 and 0.737 for fecal calprotectin, CRP, ESR and AGP, respectively. There was a strong correlation between the fecal calprotectin concentration and the endoscopic gradings for UC (r = 0.866, P < 0.001). CONCLUSION: Calprotectin in the patient's feces can reflect the disease activity of UC and can be used as a rational fecal marker for intestinal inflammation in clinical practice. This kind of marker is relatively precise, simple and noninvasive when compared with other commonly-used markers such as CRP, ESR and AGP.

Xiang JY, Ouyang Q, Li GD. · Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu 610041, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #18001547 No free full text.

Abstract: OBJECTIVES: To explore the possibility and clinical application value of fecal lactoferrin as a marker of the activity of ulcerative colitis (UC). METHODS: Specimens of feces were collected from 66 UC patients and 20 healthy persons or irritable bowel syndrome patients. ELISA was used to measure the concentration of lactoferrin in feces, and CRP and ESR were also measured. The disease activity of UC was determined by Mayo criteria. RESULTS: The fecal lactoferrin concentration of the patients with active UC was (61.6 +/- 4.8) microg/g, significantly higher than that of the patients with inactive UC and the controls [(7.9 +/- 1.1) microg/g and (3.0 +/- 0.5) microg/g, both P < 0.01], and the fecal lactoferrin concentration of the patients with inactive UC group was also significantly higher than that of the controls (P < 0.05). The higher the grade of activity of disease the higher the concentration of lactoferrin (P < 0.05 or P < 0.01). The area under curve of receiver operating characteristic (AUCROC) of fecal lactoferrin was 0.982, significantly larger than those of the CRP and ESR (0.740 and 0.692 respectively, both P < 0.01). However, there was no significant difference in AUCROC between CPR and ESR. The fecal lactoferrin concentration was positively correlated with the endoscopic grades of UC (r = 0.871, P < 0.01). CONCLUSION: Lactoferrin in feces reflects the disease activity of UC and is a rational fecal marker of intestinal inflammation for clinical application. A precise, simple, and noninvasive method, lactoferrin examination is better than common clinically used markers, such as CRP and ESR.