Diameters of left gastric vein and its originating vein on magnetic resonance imaging in liver cirrhosis patients with hepatitis B: Association with endoscopic grades of esophageal varices.

AIM: To determine whether diameters of the left gastric vein (LGV) and its originating vein are associated with endoscopic grades of esophageal varices. METHODS: Ninety-eight liver cirrhotic patients with hepatitis B undergoing magnetic resonance (MR) portography, and upper gastrointestinal endoscopy for grading esophageal varices were enrolled. Diameters of the LGV and its originating vein - the splenic vein (SV) or portal vein (PV) - were measured on MR imaging. Statistical analyses were performed to identify the association of the diameters with the endoscopic grades. RESULTS: Univariate analysis showed that the SV was predominantly the originating vein of the LGV, and diameters of the LGV and SV were associated with grades of esophageal varices. Diameters of the LGV (P = 0.023, odds ratio [OR] = 1.583) and SV (P = 0.012, OR = 2.126) were independent risk factors of presence of the varices. Cut-off LGV diameters of 5.1 mm, 5.9 mm, 6.6 mm, 7.1 mm, 7.8 mm and 5.8 mm; or cut-off SV diameters of 7.3 mm, 7.9 mm, 8.4 mm, 9.5 mm, 10.7 mm and 8.3 mm, could discriminate grades 0 from 1, 0 from 2, 0 from 3, 1 from 3, 2 from 3, and 0-1 from 2-3, respectively. CONCLUSION: Diameters of the LGV and SV are associated with endoscopic grades of esophageal varices.

Parthenolide, an inhibitor of the nuclear factor-κB pathway, ameliorates dextran sulfate sodium-induced colitis in mice.

BACKGROUND: Activation of nuclear factor-kappa B (NF-κB), which controls transcription of various pro-inflammatory cytokine genes, has been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Parthenolide, a sesquiterpene lactone compound isolated from extracts of the herb Feverfew (Tanacetum parthenium), has been demonstrated to be a potent inhibitor of NF-κB activation. This study was designed to investigate the effects of parthenolide on an experimental murine colitis model. MATERIALS AND METHODS: Experimental colitis was induced by dextran sulfate sodium (DSS), and mice were divided into 3 groups: normal control, DSS+saline, and DSS+parthenolide. The disease activity index (DAI) and histological score were observed. The tumor necrosis factor (TNF)-α and interleukin (IL)-1ß levels were measured by enzyme-linked immunosorbent assay. Phospho-IκBα, IκBα and phospho-NF-κB p65 expression were assessed by western blot analysis. Myeloperoxidase (MPO) activity was determined by using MPO assay kit. RESULTS: Administration of parthenolide significantly reduced the severity of DSS-induced colitis as assessed by DAI and histological score, and resulted in downregulation of MPO activity and phospho-NF-κB p65 expression by the blockade of phosphorylation and subsequent degradation of IκB protein, strikingly reduced the production of TNF-α and IL-1ß. CONCLUSION: Parthenolide exerts beneficial effects in experimental colitis and may therefore provide a useful therapeutic approach for the treatment of UC.

[Chemoprevention of Barrett's esophagus by celecoxib in rats].

OBJECTIVE: To examine the chemopreventive effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib for Barrett's esophagus in rats. METHODS: Fifty 8-week-old male Sprague Dawley rats underwent esophagojejunostomy to induce Barrett's esophagus model. Four weeks after operation the animals were given celecoxib 10 mg/(kg*d(-1))(celecoxib group), or saline 1 ml (control group). Another 10 rats were sham operation group. All animals were sacrificed at 20 week after surgery. The degree of inflammation, Barrett's esophagus, adenocarcinoma, COX-2 expression and PGE(2) of animals were assessed. RESULT: Among 60 rats, 6 rats died in celecoxib group, 8 rats died in control group, 1 rat died in sham operation group, and 45 (75%) rats completed the study. The incidence of mild, moderate and severe degree esophageal inflammation in celecoxib group and control group was 14/19(73.68%), 4/19(21.05%), 1/19(5.26%); 4/17(23.53%), 5/17(29.41%), 8/17(47.06%)(P<0.05), respectively. The incidence of Barrett's esophagus was 7/19(36.84%), 13/17(76.47%) in two group respectively(P<0.05); The incidence of Barrett's esophagus with dysplasia was 2/19(10.53%), 8/17(47.06%)(P<0.05), respectively. The expression of COX-2 was 1/7(14.29%), 10/13(76.92%)(P<0.05) in two groups. PGE2 content was significantly lower in the celecoxib group than that in control group(P<0.001). No esophageal pathological changes were found in sham operation group. CONCLUSION: Selective COX-2 inhibitors celecoxib can inhibit inflammations, development of Barrett's esophagus and esophagus adenocarcinoma.

[Establishment of reflux esophagitis models in rats].

OBJECTIVE: To establish animal models of reflux esophagitis in rats. METHODS: Seventy male Sprague Dawley rats aged 8 weeks were randomly divided into 4 groups: in Group A (n=20) esophagojejunostomy was performed to induce a gastro-jejuno-esophageal reflux; in Group B (n=20) esophagoduodenostomy was performed to induce a gastro-duodeno-esophageal reflux; in Group C (n=20) total gastrectomy plus esophagojejunostomy was performed to induce a jejuno-esophageal reflux; in Group D (n=10) only was performed sham operation (control). RESULT: Among 70 rats, 6 died in Group A, 7 died in Group B, 6 died in Group C, and 72.9 %(51/70) animals were completed in the study. After 12 weeks the incidence of esophageal inflammation was 100.0%; in Groups A, B and C erosion occurred in 11/14 (78.6%), 10/13 (76.9%), 3/14 (21.4%) of animals, respectively; squamous dysplasia was in 10/14 (71.4%), 10/13 (76.9%), 5/14 (35.7%) of rats, respectively; Barrett's esophagus was in 6/14 (42.9%), 5/13 (38.5%), 1/14 (7.1%), respectively. One esophageal adenocarcinoma was found in Group A; no histological changes were observed in Group D. CONCLUSION: The animal models of reflux esophagitis can be induced by esophagojejunostomy, esophagoduodenostomy or total gastrectomy plus esophago-jejunostomy in rats; and the former two surgical modalities are better than the later.

Tetrandrine ameliorates dextran-sulfate-sodium-induced colitis in mice through inhibition of nuclear factor -kappaB activation.

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.

Amelioration of murine dextran sulfate sodium-induced colitis by nuclear factor-kappaB decoy oligonucleotides.

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.

Clinical value of fecal calprotectin in determining disease activity of ulcerative colitis.

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.

[Significance of fecal lactoferrin in evaluation of disease activity in ulcerative colitis].

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.