A survey of seroepidemiology of toxoplasmosis

The article reports the result of serological investigation on toxoplasmosis among human,animaland fowl populations in Huimin District,Shandong Province.2269 samples from 1471 people,133pigs,343 sheeps,127 goats,75 chickens and 120 rabbits were tested by IHA method.There were 7％positives found in human,2.5～11.3％ in domestic animals and fowls.with the highest incicencein pigs.There are marked difference in incidences between the group of farmers,cadres and the group     

Acknowledgments to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and time to the peer review, a critical process to ensure the quality of World Journal of Gastroenterology. The editors and authors of the articles submitted to the journal are grateful to the following reviewers for evaluating the articles (including those were published and those were rejected in this issue) during the last editing period of time.     

Acknowledgements to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and timeto the peer review,a critical process to ensure the qualityof World Journal of Gastroenterology.The editors andauthors of the articles submitted to the joumal are gratefulto the following reviewers for evaluating the articles(including those were published and those were rejectedin this issue) during the last editing period of time.     

Acknowledgments to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and time to the peer review,a critical process to ensure the quality of World Journal of Gastroenterology. The editors and authors of the articles submitted to the journal are grateful to the following reviewers for evaluating the articles (including those published in this issue and those rejected for this issue) during the last editing time period.     

Acknowledgements to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and timeto the peer review,a critical process to ensure the qualityof World Journal of Gastroenterology.The editors andauthors of the articles submitted to the journal are gratefulto the following reviewers for evaluating the articles(including those were published and those were rejectedin this issue) during the last editing period of time.     

Acknowledgments to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and time to the peer review, a critical process to ensure the quality of World Journal of Gastroenterology. The editors and authors of the articles submitted to the journal are grateful to the following reviewers for evaluating the articles (including those were published and those were rejected in this issue) during the last editing period of time.     

Acknowledgments to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and time to the peer review, a critical process to ensure the quality of World Journal of Gastroenterology. The editors and authors of the articles submitted to the journal are grateful to the following reviewers for evaluating the articles (including those published in this issue and those rejected for this issue) during the last editing time period.     

Acknowledgments to Reviewers of World Journal of Gastroenterology

Many reviewers have contributed their expertise and time to the peer review, a critical process to ensure the quality of World Journal of Gastroenterology. The editors and authors of the articles submitted to the journal are grateful to the following reviewers for evaluating the articles (including those published in this issue and those rejected for this issue) during the last editing time period.     

Ameliorative effects of sodium ferulate on experimental colitis and their mechanisms in rats

AIM: To investigate the ameliorative effects of sodium ferulate (SF) on acetic acid-induced colitis and their mechanisms in rats.METHODS: The colitis model of Sprague-Dawley rats was induced by intracolon enema with 8 % (WV) of acetic acid.The experimental animals were randomly divided into model control, 5-aminosalicylic acid therapy group and three dose of SF therapy groups. The 5 groups were treated intracolonically and daily (8:00 am) for 7 days 24 h following the induction of colitis. A normal control group of rats clystered with normal saline instead of acetic acid was also included in the study.Pathological changes of the colonic mucosa were evaluated by the colon mucosa damage index (CMDI) and the histopathological score (HS). The insulted colonic mucosa was sampled for a variety of determinations at the end of experiment when the animals were sacrificed by decapitation.Colonic activities of myeloperoxidase (MPO) and superoxide dismutase (SOD), and levels of malondialdehyde (MDA)and nitric oxide (NO) were assayed with ultraviolet spectrophotometry. Colonic contents of prostaglandin E2 (PGE2) and thromboxane B2 (TXB2)were determined by radioimmunoassay. The expressions of inducible nitric oxide synthase (iNOS), cyclo-oxygenase-2 (COX-2) and nuclear factor kappa B (NF-κB) p65 proteins in the colonic tissue were detected with immunohistochemistry.RESULTS: Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in the animals clystered with acetic acid, which manifested as the significant increase of CMDI, HS, MPO activities, MDA and NO levels,PGE2 and TXB2 contents, as well as the expressions of iNOS,COX-2 and NF-κB p65 proteins in the colonic mucosa,although the colonic SOD activity was significantly decreased compared with the normal control (CMDI: 2.9±0.6 vs0.0±0.0;HS: 4.3±0.9 vs0.7±1.1; MPO: 98.1±26.9 vs24.8±11.5; MDA:57.53±12.36 vs9.21±3.85; NO: 0.331±0.092 vs0.176±0.045;PGE2: 186.2±96.2 vs 42.8±32.8; TXB2: 34.26±13.51 vs 8.83±3.75; iNOS: 0.365±0.026 vs0.053±0.015; COX-2:0.296±0.028 vs0.034±0.013; NF-κB p65:0.314±0.026 vs 0.039±0.012; SOD: 28.33±1.17 vs36.14±1.91; P<0.01).However, these parameters were found to be significantly ameliorated in rats treated locally with SF at the given dose (CMDI: 1.8±0.8, 1.6±0.9; HS: 3.3±0.9, 3.1±1.0; MPO:63.8±30.5, 36.2±14.2; MDA: 41.84±10.62, 37.34±8.58; NO:0.247±0.042; 0.216±0.033; PGE2: 77.2±26.9, 58.4±23.9;TXB2:18.07±14.83; 15.52±8.62; iNOS:0.175±0.018, 0.106±0.019;COX-2: 0.064±0.018, 0.056±0.014; NF-κBp65: 0.215±0.019,0.189±0.016; SOD: 32.15±4.26, 33.24±3.69; P<0.05-0.01).amelioration of colonic mucosal injury as evaluated by CMDI and HS.CONCLUSION: Administration of SF intracolonically may have significant therapeutic effects on the rat model of colitis induced by acetic acid enema, which was probably due to the mechanism of antioxidation, inhibition of arachidonic acid metabolism and NF-κB expression.     

A comparative analysis of two models of colitis in rats.

Two models of colitis produced in rats that have received significant attention over the past few years are the acetic acid and trinitrobenzene sulfonic acid (TNBS) models. The objective of this study was to quantify and compare the temporal relationship among mucosal permeability, epithelial injury, and inflammation induced by acetic acid, ethanol (vehicle), ethanol plus TNBS (unbuffered, pH 1.0), and ethanol plus TNBS (pH 7.4). Data obtained show that the inflammation induced by these four irritants results from caustic injury to the colonic epithelium and interstitium as measured by the rapid and dramatic increases in mucosal permeability and tissue water content as well as by histological analysis. The injurious nature of TNBS was confirmed in a separate series of studies showing that buffered TNBS (pH 7.4), in the absence of ethanol, is toxic to cultured rat intestinal epithelial cell monolayers. Only after 1-2 days of the initial insult, were signs of classical inflammation observed, including increases in colonic myeloperoxidase activity (neutrophil infiltration) and colon weight as well as hyperemia and mucosal ulcerations. Although ethanol plus TNBS (pH 1.0 or 7.4) tended to produce higher mucosal permeabilities (epithelial cell injury) at 1-2 weeks after the enemas than acetic acid or ethanol groups, only the ethanol plus TNBS (pH 7.4) permeabilities were found to be significantly enhanced. In addition, all four groups showed significant elevations in colonic myeloperoxidase activity and colon weight at 1-2 weeks after enema. It is suggested that these models of colitis are useful to study events that occur at the time of inflammation and repair. However, these models may have significant limitations in understanding events that initiate inflammation of the intestine in human inflammatory bowel disease.     

Protective effect of angelica sinensis polysaccharide on experimental immunological colon injury in rats

AIM: To study the effect of angelica sinensis polysaccharide (ASP) on immunological colon injury and its mechanisms in rats.METHODS: Immunological colitis model of rats was induced by intracolon enema with 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) and ethanol. The experimental animals were randomly divided into normal control, model control, 5-aminosalicylic acid therapy groups and three doses of ASP therapy groups. The 6 groups were treated intracolonically with normal saline, normal saline, 5-aminosalicylic acid (100 mg.kg-1), and ASP daily (8:00 am) at the doses of 200, 400 and 800 mg.kg-1 respectively for 21 days 7 d following induction of colitis. The rat colon mucosa damage index (CMDI), the histopathological score (HS), the score of occult blood test (OBT), and the colonic MPO activity were evaluated. The levels of SOD, MDA, NO, TNF-α, IL-2 and IL-10 in colonic tissues were detected biochemically and immunoradiometrically. The expressions of TGF-β and EGF in colonic tissues were also determined immunochemically.RESULTS: Enhanced colonic mucosal injury, inflammatory response and oxidative stress were observed in colitis rats,which manifested as significant increases of CMDI, HS, OBT,MPO activity, MDA and NO contents, as well as the levels of TNF-α and IL-2 in colonic tissues, although colonic TGF-β protein expression, SOD activity and TL-10 content were significantly decreased compared with the normal control (P＜0.01). However, these parameters were found to be significantly ameliorated in colitis rats treated intracolicly with ASP at the doses of 400 and 800 mg@kg-1 (P＜0.05-0.01).Meantime, colonic EGF protein expression in colitis rats was remarkably up-regulated.CONCLUSION: ASP has a protective effect on immunological colon injury induced by TNBS and ethanol enema in rats,which was propably due to the mechanism of antioxidation,immunomodulation and promotion of wound repair.     

Butyrate enema therapy stimulates mucosal repair in experimental colitis in the rat.

BACKGROUND--The short chain fatty acid (SCFA) butyrate provides energy for colonocytes, stimulates colonic fluid and electrolyte absorption and is recognised as an effective treatment for multiple types of colitis. AIM--To examine the impact of butyrate enema therapy on the clinical course, severity of inflammation, and SCFA stimulated Na+ absorption in a chronic experimental colitis. METHODS--Distal colitis was induced in rats with a trinitrobenzenesulphonic acid (TNBS) enema. Five days after induction, rats were divided into groups to receive: no treatment, saline enemas, or 100 mM Na-butyrate enemas daily. On day 24, colonic damage score and tissue myeloperoxidase (MPO) activity were evaluated. Colon was mounted in Ussing chambers and Na+ transport and electrical activities were measured during a basal period and after stimulation with 25 mM butyrate. RESULTS--In the untreated and the saline enema treated TNBS groups, diarrhoea and extensive colonic damage were seen, associated with increased tissue MPO activities and absent butyrate stimulated Na+ absorption. In contrast, in the butyrate enema treated TNBS group, diarrhoea ceased, colonic damage score improved, and tissue MPO activity as well as butyrate stimulated Na+ absorption recovered to control values. CONCLUSION--Butyrate enema therapy stimulated colonic repair, as evidenced by clinical recovery, decreased inflammation, and restoration of SCFA stimulated electrolyte absorption.     

青黛颗粒对溃疡性结肠炎大鼠结肠黏膜MUC2和iNOS基因表达的影响

目的:观察青黛颗粒对TNBS诱导的溃疡性结肠炎(UC)大鼠结肠黏膜黏蛋白(MUC2)及诱导型一氧化氮合成酶(iNOS)基因表达的影响,探讨其治疗UC的可能作用机制.方法:将54只SD实验大鼠随机分为正常对照组、模型对照组、阳性药物治疗组(SASP,500 mg/kg)、青黛颗粒600、900、1 200 mg/kg治疗组.造模后第3天开始灌胃给药,共给药10d.实验第14天,处死大鼠,剖取其病变结肠组织,比较各组大鼠的DAI积分和CMDI评分,用逆转录聚合酶链反应(RT-PCR)法检测MUC2及iNOS基因的表达.结果:较模型组青黛颗粒900、1200 mg/kg治疗组能显著降低实验大鼠DAI积分和CMDI评分,上调结肠组织中MUC2的基因表达(2.06±0.70 vs 1.24±0.47;2.34±0.86 vs 1.24±0.47.均P<0.01),且青黛颗粒1 200 mg/kg治疗组能下调iNOS的基因表达(0.35±0.12vs 0.62±0.31.P<0.05).结论:青黛颗粒可能通过上调结肠黏膜MUC2的基因表达并下调iNOS的基因表达而起到抗TNBS诱导的大鼠溃疡性结肠炎的作用.     

Cyclooxygenase-2 inhibition and experimental colitis: beneficial effects of phosphorothioated antisense oligonucleotide and meloxicam

BACKGROUND: The effects of cyclooxygenase-2 (cox-2) inhibition by a cox-2 selective antisense phosphorothioated oligonucleotide (AS) and meloxicam were examined in experimental colitis. METHODS: Colitis was induced by trinitrobenzenesulphonic acid (TNBS) and acetic acid (Hac) separately in male Sprague-Dawley rats. Both groups of animals were treated daily intraperitoneally with AS and a mismatched control oligo (CO) (3 mg/kg), and orally with meloxicam (7.5 mg/kg) 1 h before induction of colitis. The animals were killed on day 4 (Hac) and on day 5 (TNBS). Tissue samples from colon, ileum, liver, kidney and spleen were collected for mRNA, myeloperoxidase activity (MPO), prostaglandin E2 (PGE2) estimation and for histology, and blood samples for PGE2, thromboxane B2 (TxB2) and TNF-alpha. RESULTS: Both TNBS and Hac increased colonic MPO activity, PGE2 concentrations and infiltration of colonic wall by inflammatory cells. Serum levels of TNF-alpha were increased in both models, whereas PGE2 was increased only in TNBS colitis. Only meloxicam suppressed the level of PGE2 significantly below the basal level. The animals in both models also showed splenomegaly. The colitis-induced changes were significantly suppressed by the treatment of the test compounds but not by the CO. Cox-2 mRNA but not cox-1 was decreased by the AS, but not by meloxicam or in CO-treated colitic animals. CONCLUSION: The findings demonstrate comparable beneficial effects of the cox-2 selective antisense oligonucleotide and meloxicam, which seem to be mediated by a combined inhibition of both PGE2 and TNF-alpha in the present models of colitis.     

Cyclooxygenase-2 Inhibition and Experimental Colitis: Beneficial Effects of Phosphorothioated Antisense Oligonucleotide and Meloxicam

Background: The effects of cyclooxygenase-2 (cox-2) inhibition by a cox-2 selective antisense phosphorothioated oligonucleotide (AS) and meloxicam were examined in experimental colitis. Methods: Colitis was induced by trinitrobenzenesulphonic acid (TNBS) and acetic acid (Hac) separately in male Sprague-Dawley rats. Both groups of animals were treated daily intraperitoneally with AS and a mismatched control oligo (CO) (3 mg/kg), and orally with meloxicam (7.5 mg/kg) 1 h before induction of colitis. The animals were killed on day 4 (Hac) and on day 5 (TNBS). Tissue samples from colon, ileum, liver, kidney and spleen were collected for mRNA, myeloperoxidase activity (MPO), prostaglandin E 2 (PGE 2 ) estimation and for histology, and blood samples for PGE 2 , thromboxane B 2 (TxB 2 ) and TNF- α. Results: Both TNBS and Hac increased colonic MPO activity, PGE 2 concentrations and infiltration of colonic wall by inflammatory cells. Serum levels of TNF- α were increased in both models, whereas PGE 2 was increased only in TNBS colitis. Only meloxicam suppressed the level of PGE 2 significantly below the basal level. The animals in both models also showed splenomegaly. The colitis-induced changes were significantly suppressed by the treatment of the test compounds but not by the CO. Cox-2 mRNA but not cox-1 was decreased by the AS, but not by meloxicam or in CO-treated colitic animals. Conclusion: The findings demonstrate comparable beneficial effects of the cox-2 selective antisense oligonucleotide and meloxicam, which seem to be mediated by a combined inhibition of both PGE 2 and TNF- α in the present models of colitis.     

Effects of Changtai granules, a traditional compound Chinese medicine, on chronic trinitrobenzene sulfonic acid-induced colitis in rats

AIM: To study the effects of Changtai granules (CTG), a traditional compound Chinese medicine, on chronic trinitrobenzene sulfonic acid-induced colitis in rats. METHODS: Healthy adult Sprague-Dawley (SD) rats of both sexes, weighing 250-300 g, were employed in the present study. The rat colitis models were induced by 2, 4,6-trinitrobenzene sulfonic acid (TNBS) enemas at a concentration of 100 mg/kg in 50% ethanol. The experimental animals were randomly divided into dexamethasone (DX) treatment, CTG treatment, and model control groups, which were intracolicly treated daily with DX (0.2 mg/kg), CTG at doses of 2.9, 5.7 and 11.4 g crude drug/kg, and the equal amount of saline respectively from 6 h following induction of the colitis in rats inflicted with TNBS to the end of study. A normal control group of rats treated without TNBS but saline enema was also included in the study. After 3 wk of treatment, the animals were assessed for colonal inflammatory and ulcerative responses with respect to mortality, frequency of diarrhea, histology and myeloperoxidase activity (MPO). RESULTS: The therapeutic effect of CTG on ulcerative colitis (UC) was better than DX. CTG effectively inhibited the activity of granulocytes, macrophages and monocytes in a dose-dependent manner. Also it reduced MPO and formation of inflammation in colonic mucosal tissue. Furthermore, administration of CTG significantly prevented body mass loss and death, and decreased frequency of diarrhea in UC rats, when compared with the model control group rats. CONCLUSION: CTG would prove to be an ideal drug for chronic UC, and is warranted to be studied further.     

Therapeutic effect of phenantroline in two rat models of inflammatory bowel disease.

BACKGROUND: Phenantroline is a zinc-chelator that inhibits biological activities of matrix metalloproteinases (MMPs). Over-expression of MMPs can accelerate tissue destruction and disrupt subsequent tissue repair. The effects of phenantroline in two rat models of inflammatory bowel disease (IBD) are evaluated: transmural colitis induced by trinitrobenzensulphonic acid (TNBS) and distal colitis caused by dextran sulphate sodium (DSS). METHODS: Transmural colitis was induced by TNBS in two groups of 15 rats each, and distal colitis was induced by DSS in two other groups of 15 rats each. Phenantroline was administered by oral gavage at 20 mg kg(-1) day(-1) to the test groups, whereas matched control groups received oral vehicle. On the last day of dosing, rats were subjected to intracolonic dialysis under anaesthesia for assessment of luminal eicosanoid release (PGE2, TXB2 and LTB4) and euthanized. Colons were removed and lesions were blindly scored according to macroscopic and histological scales. Myeloperoxidase (MPO) activity was measured in homogenates of colonic tissue. RESULTS: In the TNBS model, phenantroline treatment significantly reduced colonic strictures; in the DSS model, phenantroline significantly decreased scores of epithelial injury. In both models, the levels of PGE2, TXB2 and LTB4 and tissue MPO were not significantly altered. CONCLUSIONS: Although phenantroline did not modify the activity of inflammatory mediators, this compound substantially reduced intestinal injury associated with tissue remodelling.     

Establishment of a trinitrobenzene sulfonic acid‐induced rat colitis model

OBJECTIVE : To set up a trinitrobenzene sulfonic acid (TNBS)‐induced colitis model in the rat and to assess its value in research studies of inflammatory bowel disease (IBD). METHODS : A 0.85‐mL enema containing 30 mg TNBS dissolved in 50% ethanol was instilled into the rat colon to induce distal colitis. Control rats were instilled with 50% ethanol or TNBS/saline alone. Macroscopic histological changes of the colon and myeloperoxidase (MPO) activity of the mucosa were evaluated. RESULTS : One week after the TNBS/ethanol enema, hyperemia, edema and ulceration of the colonic mucosa appeared with predominant infiltration of polymorphonuclear leukocytes in the distal colon. Four weeks after TNBS/ethanol enema, ulcers had healed macroscopically and lymphocytes and plasma cells became predominant. The tissue MPO activity increased on the first day after the TNBS/ethanol enema and this increase in MPO activity lasted for 3 weeks, but declined 4 weeks after the TNBS/ethanol enema. In contrast, macroscopic, histological changes and MPO activity returned to normal levels in control rats within the first week. CONCLUSIONS : Trinitrobenzene sulfonic acid/ ethanol‐induced rat distal colitis is an ideal model of IBD and may serve as a tool for the investigation of the pathogenesis of and effects of pharmaceuticals on IBD.