Effects Of Sulfasalazine Research Articles

Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease

Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment (n = 5) to no treatment (n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.

Effectiveness of sulfasalazine and methotrexate in 1102 DMARD-naive patients with early RA

To compare baseline characteristics, responses and drug survival in patients with early RA starting SSZ or MTX in a real-life setting. The analyses included DMARD-naïve patients with RA (disease duration ≤ 1 year) starting SSZ or MTX. Three- and 6-month effectiveness was compared by unadjusted analysis and with adjustment for propensity score quintile. In addition, effectiveness in SSZ- and MTX-treated patients matched for RF status and baseline DAS-28 was compared. SSZ-treated patients (n = 175) had lower baseline disease activity than patients treated with MTX (n = 927) [mean 28-joint DAS (DAS-28) 4.4 vs 5.0, P < 0.001], and were less often RF positive (50 vs 61%, P = 0.006). Six-month mean ΔDAS-28 was smaller with SSZ than MTX (-1.0 vs -1.5, P = 0.003); the difference was not significant after adjustment for propensity score quintile (P = 0.36). For SSZ/MTX, 3-month ACR50 and European League Against Rheumatism (EULAR) good responses were 9/23% (P < 0.001) and 24/31% (P = 0.14), respectively. Three-year drug survival was superior for MTX (P < 0.001) and estimated 1-year survival rates were 42/75% for SSZ/MTX. In patients matched for baseline DAS-28 and RF, mean ΔDAS-28 (MTX -1.2, P = 0.55 vs SSZ) and EULAR good responses (39 vs 37%, P = 0.74) were similar at 6 months; drug survival was superior for MTX (P < 0.001). Patients treated with SSZ as first DMARD were more often RF negative and had lower baseline disease activity. Drug survival was superior for MTX, and effectiveness was greater with MTX than with SSZ although the difference was reduced when adjusting for differences in baseline characteristics.

The effect of sulfasalazine on homocysteine metabolism in vivo

Sulfasalazine (SSZ) is a disease‐modifying antirheumatic drug (DMARD) commonly used in the treatment of rheumatoid arthritis that inhibits intestine folate absorption and multiple folate‐dependent enzymes. The objective of the present study was to systematically investigate the impacts of long‐term SSZ treatment on homocysteine metabolism in vivo. C57BL/6J mice received either sterile 0.5% cellulose i.p. (vehicle, control group) or SSZ (80 mg/kg/day) for 8 weeks. Folate, S‐adenosyl methionine (adoMet), S‐adenosylhomocysteine (adoHcy) and homocysteine were determined in blood and tissues. Whole blood adoMet levels were significantly elevated compared to subjects on other DMARDs (1807 ± 1346, vs. 330 ± 861, p &lt; 0.001), suggesting that SSZ may increase adoMet synthesis or decrease adoMet utilization. Furthermore, whole blood adoMet levels significantly correlated with the weekly dosage of SSZ (r = 0.34, p = 0.002) in patients receiving SSZ (n = 63).SSZ did not alter adoMet, adoHcy, methionine adenosyltransferase (MAT) activity and methylated cytidine content of DNA (dMC%) in mice liver or kidney. SSZ treatment increased whole blood adoMet level by induction of the methionine adenosyltransferase activity in erythrocytes in mice. In the present study we demonstrated the novel finding of a direct inducing effect of SSZ treatment on adoMet synthesis and adoMet synthase activity in blood.Grant Funding Source: ASN

Effect of Sulfasalazine on Renal Ischemia/Reperfusion Injury in Rats

Renal ischemia/reperfusion (I/R) occurs during shock and transplant procedures, greatly affecting outcome. A definitive treatment has not been found. One of the pathophysiological bases of renal I/R injury is the activation of the transcription factor nuclear factor-kappaB (NF-KappaB). We studied the effects of sulfasalazine (SFZ), a NF-kappaB inhibitor, over renal injury in a bilateral renal I/R model in rats. Ten male Wistar rats were subjected to bilateral renal I/R for 45 min followed by 24 h of reperfusion. Half of these received 100 mg/kg SFZ orally before the induction of I/R, while the others received only saline. Five rats served as sham-operated controls. At the end of the reperfusion period, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN), P-selectin, tumor necrosis factor-alpha (TNF-alpha), intracellular adhesion molecule-1 (ICAM-1), and endothelin-1 (ET-1) concentrations were determined in serum, and renal samples were taken for histological evaluation. After renal I/R, AST, LDH, BUN, TNF-alpha, ICAM-1, and ET-1 serum levels were significantly increased, and tubules were severely damaged on histological analysis, compared to sham controls. SFZ treatment reduced the AST, LDH, BUN, TNF-alpha, and ET-1 elevations, as well as the tubular damage, induced by renal I/R. Serum ICAM-1 and P‐selectin were unchanged. These results show that SFZ has a protective effect over renal IR injury. The modulation of adhesion molecules probably does not play a part in these effects, but TNF-alpha and ET-1 modulation could be partly responsible for the effects we observed.

Genomic analysis of sulfasalazine effect in experimental colitis is consistent primarily with the modulation of NF-κB but not PPAR-γ signaling

Sulfasalazine (SAZ) is a widely used drug in inflammatory bowel disease patients but its mechanism of action is incompletely understood. The objective of our study was to further characterize SAZ mechanism by studying its effect on the colonic transcriptome in a suitable preclinical model of inflammatory bowel disease. The trinitrobenzenesulfonic acid model of colitis in rats was used. The effect of SAZ on mRNA expression was assessed with Affymetrix Rat Expression 230 2.0 arrays used in triplicate (sextuplicate for controls), validated in separate samples with quantitative reverse-time PCR analysis. Some nongenomic experiments were also carried out. SAZ (500 mg/kg) had a marked anti-inflammatory effect as expected, which was correlated with a dramatic impact on colonic gene expression. In addition to immune/inflammatory genes, SAZ responsive genes were involved in distinct metabolic and signaling pathways. The effect of sulfasalazine was generally of normalization of colitis-modulated genes to control levels, with very few exceptions. Postgenomic validation showed an excellent correlation with microarray data and seemed to be slightly more sensitive. SAZ generally modulated the expression of nuclear factor-kappaB-driven genes. SAZ was also shown to inhibit IkappaB-alpha phosphorylation in rat primary splenocytes and in HT29 and IEC18 cells. In contrast, SAZ had only a modest effect on peroxisome proliferator-activated receptor (PPAR)-gamma-regulated genes and it was confirmed to induce PPAR-gamma in enterocytes but not splenocytes. Mechanistically, our data are consistent primarily with nuclear factor-kappaB inhibition, and there is little evidence of a prominent role of activation of PPAR-gamma receptors or antioxidative actions.

ORIGINAL ARTICLE: Effect of Sulfasalazine on Basal and Bacteria‐Stimulated Interleukin‐8 Production by Endocervical Epithelial Cells

Problem Sulfasalazine (SASP) inhibits lipopolysaccharide‐induced nuclear‐factor kappa B activation and interleukin‐8 (IL‐8) production by cultured explants of placenta, amnion and choriodecidua. Bacteria‐induced IL‐8 production in the cervix is a potential mechanism for premature cervical ripening that may lead to preterm birth. Our objective was to determine if SASP inhibits IL‐8 production by endocervical cells stimulated with bacterial pathogens associated with preterm birth.Method of study Human endocervical cells were incubated with 0–1.6 mm SASP and then stimulated with Ureaplasma parvum, Escherichia coli, or Gardnerella vaginalis. Conditioned medium was then harvested and production of IL‐8 was quantified by ELISA. Viability of the cells was ascertained at the end of the experiment with the MTT‐assay.Results At the highest concentration tested (1.6 mm), SASP significantly inhibited IL‐8 production by cultures stimulated with E. coli (P &lt; 0.001), U. parvum (P &lt; 0.001), and G. vaginalis (P &lt; 0.001). Viability of the cells, however, was significantly reduced by SASP at 0.8 and 1.6 mm in both the presence and absence of bacteria for all experiments.Conclusion Although high concentrations of SASP inhibit IL‐8 production by cultures of endocervical cells stimulated with pathogens associated with preterm birth, this effect may be because of toxicity of the antibiotic on the cells.

The Role of Nuclear Factor Kappa B in Lens Epithelial Cell Proliferation Using a Capsular Bag Model

Purpose: This study was performed to elucidate the role of nuclear factor ĸB (NF-ĸB) in lens epithelial cell proliferation in the capsular bag model for this study. Methods: Capsular bags were prepared from porcine eyes and cultured in a 5% CO₂ atmosphere at 37°C. NF-ĸB translocation was confirmed by immunohistochemistry and Western blot analysis. The effects of sulfasalazine and SN50 peptide, inhibitors of NF-ĸB activation, were observed by light microscopy and scanning electron microscopy. Results: NF-ĸB was found in the cytoplasm of nonproliferated lens epithelial cells. However, NF-ĸB moved to the nucleus in proliferation cells, proliferating-cell-nuclear-antigen-positive cells. This translocation was inhibited by treatment with sulfasalazine or NF-ĸB SN50 peptide. These inhibitors also blocked lens epithelial cell migration from the equatorial to the posterior capsule. Conclusion: NF-ĸB controls proliferation and regulates the growth of lens epithelial cells. In this study, sulfasalazine and NF-ĸB SN50 peptide inhibited cell proliferation in the capsular bag model. These results suggest that the regulation of NF-ĸB in lens epithelial cells may modulate posterior capsule opacification.

Ursodeoxycholic Acid versus Sulfasalazine in Colitis-Related Colon Carcinogenesis in Mice

Inflammation influences carcinogenesis. In the current study, we investigated whether ursodeoxycholic acid (UDCA) can inhibit colitis-related mouse colon carcinogenesis and compared it with the effects of sulfasalazine. Male CD-1 mice were given a single i.p. injection of azoxymethane followed by 1-week oral exposure of 1% dextran sodium sulfate in drinking water. They are then maintained on a basal diet mixed with UDCA (0.016%, 0.08%, or 0.4%) or sulfasalazine (0.05%) for 17 weeks. At week 20, the tumor-inhibitory effects of both chemicals were assessed by counting the incidence and multiplicity of colonic neoplasms. The immunohistochemical expression of the proliferating cell nuclear antigen labeling index in colonic epithelial malignancies was also assessed. Finally, at week 5, the mRNA expressions for cyclooxygenase-2, inducible nitric oxide synthase, peroxisome proliferator-activated receptor-gamma, and tumor necrosis factor-alpha were measured in nontumorous mucosa. Feeding the mice with UDCA at all doses significantly inhibited the multiplicity of colonic adenocarcinoma. The treatment also significantly lowered the proliferating cell nuclear antigen labeling index in the colonic malignancies. UDCA feeding reduced the expression of inducible nitric oxide synthase and tumor necrosis factor-alpha mRNA in the colonic mucosa, while not significantly affecting the expression of cyclooxygenase-2 mRNA and peroxisome proliferator-activated receptor-gamma mRNA. Sulfasalazine caused a nonsignificant reduction in the incidence and multiplicity of colonic neoplasia and did not affect these mRNA expression. Our findings suggest that UDCA rather than sulfasalazine could serve as an effective suppressing agent in colitis-related colon cancer development in mice.

Effects of sulfasalazine on sperm acrosome reaction and gene expression in the male reproductive organs of rats

Effects of sulfasalazine on sperm acrosome reaction and gene expression in the male reproductive organs of rats

Effects of sulfasalazine on biopsy mucosal pathologies and histological grading of patients with active ulcerative colitis

To investigate the mechanisms of sulfasalazine (SASP) in the treatment of ulcerative colitis (UC). Changes of pathological signs and histological grading of 106 patients with active UC were observed before and after the treatment with SASP, 1 g, thrice daily for 6 wk. The effect of SASP on the vasculitis in lamina propria was 48.2% and 17.4% in the mild active UC (P<0.001) and 68% and 26.7% in the moderate active UC (P<0.001) before and after treatment. Fibroid necrosis of vessel wall was found in one case of mild UC and two cases of moderate UC before treatment and was not found after treatment. No thrombosis was found in mild UC before and after treatment, while thrombosis was found in one case of moderate UC before treatment. The effect on mucosal glandular abnormality was 30.4% and 13.0% in mild UC (P<0.05), and 42% and 40% in moderate UC (P>0.05) before and after treatment. The rate of eosinophil infiltration was 98.2% and 80.4% in mild UC (P<0.01), and 100% and 91.1% in moderate UC (P<0.05) before and after treatment. The effect on crypt abscess was 21.4% and 4.4% in mild UC (P<0.05), and 48% and 13.3% in moderate UC (P<0.001) before and after treatment. The effect on mucosal pathohistological grading was 2.00+/-0.84 and 0.91+/-0.46 in mild UC (P<0.001), and 2.49+/-0.84 and 1.31+/-0.75 in moderate UC (P<0.001) before and after treatment. SASP can improve small vessel lesions and crypt abscesses and reduce neutrophilic and eosinophilic leukocyte infiltration in inflammatory mucosa of UC.

Effects of Sulfasalazine on Sperm Acrosome Reaction and Gene Expression in the Male Reproductive Organs of Rats

Sulfasalazine (SASP) has been reported to depress the fertility in men and experimental male animals, but the fundamental mechanisms of infertility caused by SASP are still unknown. This study was designed to investigate the mechanisms of infertility in rats treated with SASP at a dose of 600 mg/kg for 28 days, including monitoring of sperm motility using computer associated sperm analysis system and acrosome reaction by FITC-concanavalin A lectin staining. The sperm motility and acrosome reaction, which are important for fertilization, were significantly reduced by SASP. Furthermore, to investigate the molecular mechanisms of infertility induced by SASP, mRNA expression analysis in the testes was performed using cDNA microarray as a first screening. It was revealed that CD59, which is located on the acrosomal membrane and is known to be important for the reproductive function of sperm, was affected in the testes; this was also confirmed by real-time PCR analysis, but the spermatogenesis-related genes examined in this study were not affected. Therefore, we focused on CD59 and two other acrosome membrane related-genes: MCP and DAF. CD59, MCP, and DAF in the epididymides of SASP-treated rats were significantly decreased as assessed by real-time RT-PCR analysis and additionally, the expression of CD59 protein was found to be decreased by Western blotting. These results allowed us to hypothesize that the suppression of epididymal acrosomal membrane proteins synthesis with their consequent reduced incorporation to the sperm membrane leads to a depressed sperm motility and acrosome reaction, and thereby leads to infertility in SASP treated male rats.

Sulfasalazine and BAY 11-7082 Interfere with the Nuclear Factor-κB and IκB Kinase Pathway to Regulate the Release of Proinflammatory Cytokines from Human Adipose Tissue and Skeletal Muscle in Vitro

There is much evidence to indicate a role for adipocytokines in insulin resistance and/or type 2 diabetes mellitus. In experimental models, oral salicylates, through their ability to interfere with the nuclear factor-kappa B (NF-kappa B) transcription pathway, have been demonstrated to reverse insulin resistance. The aim of this study was to investigate whether NF-kappa B regulates the release of adipocytokines in human adipose tissue and skeletal muscle. Human sc adipose tissue and skeletal muscle (obtained from normal pregnant women) were incubated in the absence (control) or presence of two NF-kappa B inhibitors sulfasalazine (1.25, 2.5, and 5 mm) and BAY 11-7082 (25, 50, and 100 microm). After an 18-h incubation, the tissues were collected, and NF-kappa B p65 DNA-binding activity and I kappa B kinase (IKK-beta) and insulin receptor-beta protein expression were assessed by ELISA and Western blotting, respectively. The incubation medium was collected, and the release of TNF-alpha, IL-6, IL-8, resistin, adiponectin, and leptin was quantified by ELISA. Treatment of adipose tissue and skeletal muscle with sulfasalazine and BAY 11-7082 significantly inhibited the release of IL-6, IL-8, and TNF-alpha; NF-kappa B p65 DNA-binding activity; and IKK-beta protein expression (P < 0.05, by Newman-Keuls test). There was no effect of sulfasalazine and BAY 11-7082 on resistin, adiponectin, or leptin release. Both sulfasalazine and BAY 11-7082 increased the adipose tissue and skeletal muscle expression of insulin receptor-beta. The data presented in this study demonstrate that the IKK-beta/NF-kappa B transcription pathway is a key regulator of IL-6, IL-8, and TNF-alpha release from adipose tissue and skeletal muscle. Control of the IKK-beta/NF-kappa B pathway may therefore provide an alternative therapeutic strategy for regulating aberrant cytokine release and thereby alleviating insulin resistance in type 2 diabetes mellitus.

Effects of sulfasalazine on 6-mercaptopurine metabolism and clinical efficacy in patients with Crohn’s disease: preliminary results of a placebo-controlled randomized clinical trial

Effects of sulfasalazine on 6-mercaptopurine metabolism and clinical efficacy in patients with Crohn's disease: preliminary results of a placebo-controlled randomized clinical trial

The effect of 5-aminosalicylic acid-containing drugs on sulfide production by sulfate-reducing and amino acid-fermenting bacteria.

The toxic, bacterial metabolite sulfide is implicated in ulcerative colitis. Ulcerative colitis patients taking 5-aminosalicylic acid-containing drugs have lower fecal sulfide levels than those not taking these drugs. The effects of sulfasalazine, balsalazide, olsalazine, and 5-aminosalicylic acid on sulfide production were studied in a three-stage chemostat pulsed on days 1 to 3 with 5 g sulfasalazine (40 mM) and in pure cultures of amino acid-fermenting and sulfate-reducing bacteria. By the third day of sulfasalazine addition to the chemostat, sulfide concentrations in vessels 1 through 3 had dropped from 1.73, 1.78, and 1.43 mM to 0.01, 0.15, and 0.9 mM, respectively. In pure cultures, 50% inhibition of sulfide production from amino acids occurred at 2.5 +/- 0.05 mM for sulfasalazine, 5 +/- 0.2 mM for olsalazine, 6 +/- 1 mM for balsalazide, and more than 20 mM for 5-aminosalicylic acid. Fifty percent inhibition of sulfide production from sulfate occurred at 0.25 +/- 0.05 mM for sulfasalazine, 0.7 +/- 0.2 mM for balsalazide, and 9.0 +/- 1.0 mM for 5-aminosalicylic acid. The order of effectiveness of equimolar concentrations of drugs (most effective first) in this assay was sulfasalazine, then olsalazine (though given clinically at half the dose of other 5-aminosalicylic acid prodrugs) and balsalazide, and lastly 5-aminosalicylic acid. Inhibition of sulfide production by 5-aminosalicylic acid-containing drugs may contribute to their therapeutic effect in ulcerative colitis.

40-Year-Old Man With Anemia, Chronic Low Back Pain, and Hypoalbuminemia

40-Year-Old Man With Anemia, Chronic Low Back Pain, and Hypoalbuminemia

Reactive nitrogen species inhibit alveolar epithelial fluid transport after hemorrhagic shock in rats.

Our recent experimental work demonstrated that a neutrophil-dependent inflammatory response in the lung prevented the normal up-regulation of alveolar fluid clearance by catecholamines following hemorrhagic shock. In this study, we tested the hypothesis that the release of NO within the airspaces of the lung was responsible for the shock-mediated failure of the alveolar epithelium to respond to catecholamines in rats. Hemorrhagic shock was associated with an inducible NO synthase (iNOS)-dependent increase in the lung production of NO and a failure of the alveolar epithelium to up-regulate vectorial fluid transport in response to beta-adrenergic agonists. Inhibition of iNOS restored the normal catecholamine-mediated up-regulation of alveolar liquid clearance. Airspace instillation of dibutyryl cAMP, a stable analog of cAMP, restored the normal fluid transport capacity of the alveolar epithelium after prolonged hemorrhagic shock, whereas direct stimulation of adenyl cyclase by forskolin had no effect. Pretreatment with pyrrolidine dithiocarbamate or sulfasalazine attenuated the iNOS-dependent production of NO in the lung and restored the normal up-regulation of alveolar fluid clearance by catecholamines after prolonged hemorrhagic shock. Based on in vitro studies with an alveolar epithelial cell line, A549 cells, the effect of sulfasalazine appeared to be mediated in part by inhibition of NF-kappaB activation, and the protective effect was mediated by the inhibition of IkappaBalpha protein degradation. In summary, these results provide the first in vivo evidence that NO, released within the airspaces of the lung probably secondary to the NF-kappaB-dependent activation of iNOS, is a major proximal inflammatory mediator that limits the rate of alveolar epithelial transport after prolonged hemorrhagic shock by directly impairing the function of membrane proteins involved in the beta-adrenergic receptor-cAMP signaling pathway in alveolar epithelium.

Effects of sulfasalazine treatment on serum immunoglobulin levels in children with juvenile chronic arthritis

This article describes the effects of sulfasalazine (SSZ) treatment on serum immunoglobulin (Ig) levels in 6 children with oligoarticular - or polyarticular onset juvenile chronic arthritis (JCA). None of the children who developed dysimmunoglobulinemia during treatment showed clinical symptoms of this adverse event, in particular none developed severe infections. All patients regained normal immunoglobulin levels after discontinuing SSZ treatment. One patient with a partial IgA deficiency at the start of SSZ treatment showed a slow increase in the IgA level during treatment. During follow-up (4-6 years), one patient spontaneously developed a dysimmunoglobulinemia and one patient developed diabetes mellitus. Based on these case reports and review of the literature we advocate monitoring of serum immunoglobulin levels while on SSZ treatment.

Sulfasalazine is a potent and specific inhibitor of IKB-kinases IKKa and IKKb

Background & Aims: NF-KBlRel has been implicated in the pathogenesis of inflammatory bowel disease (IBD). Various drugs known to be effective for the treatment of IBD such as glucocorticoids and salicylates have been shown to interfere with NF-KBlRel signaling. The aim of this study was to define the molecular mechanism by which sulfasalazine inhibits NF-KB activation. Methods: The effects of sulfasalazine and its moieties on NF-KB signaling were evaluated using electromobility shift-, transfectionand immune complex kinase-assays. The direct effect of sulfasalazine on IKB kinase (IKK) activity was investigated using purified recombinant IKKaand IKKl3proteins. Results: NF-kBlRel activity induced by the overexpression of NF-KBinducing kinase (NIK), IKKa, IKKI3, or consitutively active IKKaand IKKl3mutants was inhibited in a dose dependent manner by sulfasalazine. Sulfasalazine inhibited TNFa, PMA and IL-I induced activation of endogenous IKKs in colonic epithelial and Jurkat T cells. Sulfasalazine did not affect other cell1ular kinases such as MAP-kinases JNK and p38. Sulfasalazine diminished the catalytic activity of purified IKKaand IKKl3in vitro. In contrast, the metabolic moieties of sulfasalazine, 5-aminosalicylic acid and sulfapyridine were not effective. The decrease in substrate phosphorylation by IKKaandl3is associated with a decrease of autophosphorylation of IKKs and can be antagonized by excess ATP. Conclusions: These data suggest that sulfasalazine is a competitive antagonist of ATP binding of IKKaand IKKI3. This suppression of NF-kB activation by inhibition of IKK activity may contribute to the well-known anti-inflammatory and immunosuppressive effects of sulfasalazine.

Effects of germinated barley foodstuff on dextran sulfate sodium-induced colitis in rats

Germinated barley foodstuff (GBF), derived from the aleurone and scutellum fractions of germinated barley, is rich in glutamine and low-lignified hemicellulose, and increases mucosal protein, RNA, and DNA content in the intestine when fed to normal rats. The aim of this study was to evaluate the effects of feeding GBF or germinated gramineous seeds on experimental ulcerative colitis. Sprague-Dawley rats that received 3% dextran sulfate sodium in their diets were used as an experimental colitis model. The effects of sulfasalazine, a drug used to treat inflammatory bowel disease, were compared with those of GBF. After rats had consumed diets containing GBF or various aleurone and scutellum fractions, mucosal damage; the content of mucosal protein, RNA, and DNA in the colo-rectum; and serum interleukin-8 and alpha1-acid glycoprotein levels were assessed. GBF and germinated seeds more effectively prevented bloody diarrhea and mucosal damage in colitis compared with controls and rats receiving sulfasalazine, but non-germinated samples did not have a protective effect. GBF increased mucosal protein and RNA content in the colitis model. The consumption of GBF appears to prevent inflammation in a colitis model, and its effect seems to be related to the germination process. GBF and germinated seeds have the potential to serve as nutritional therapy for ulcerative colitis.

Therapeutic Aspects of Spondyloarthropathies - A Review

In the pathogenesis of spondyloarthropathies, infection and gut inflammation are the most important external triggering factors. Early antimicrobial therapy to treat urethritis caused by Chlamydia trachomatis is effective in preventing a recurrent reactive arthritis. When the arthritis appears, a short term conventional antimicrobial therapy is unable to modify its course. In acute chlamydia arthritis, patients benefit from a prolonged (3-month) treatment with tetracycline, while such a treatment has not proved to be effective in enteroarthritis or in chronic forms of reactive arthritis. The role of sulfasalazine in the treatment of patients with spondyloarthropathies is controversial. It might modify the disease course during acute and chronic reactive arthritis, and is working for patients with ankylosing spondylitis, especially patients with peripheral arthritis. Data showing an effect of sulfasalazine in the prevention of chronic spondyloarthropathy or in modification of the long-term prognosis of ankylosing spondylitis are, however, lacking.