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PubMedDate not supplied

Aortic aneurysm repair is associated with a lower inflammatory response compared with surgery for inflammatory bowel disease.

BACKGROUND: Since the plasma cytokine profile reflects the body's inflammatory response to injury, this study was designed to prospectively observe the plasma cytokine levels in response to the degree of different sorts of abdominal surgical trauma. METHODS: Plasma levels of TNF-alpha, type I TNF receptor (p55), type II TNF receptor (p75), IL-6, IL-8, IL-10, phospholipase A(2) (PLA(2)), and haptoglobin were measured peri-operatively in patients undergoing bowel resection for inflammatory bowel disease or diverticulitis (IBD) (n = 9), elective repair of abdominal aortic aneurysm (AAA) (n = 9), or laparoscopic cholecystectomy (lap chole) (n = 9). RESULTS: The IBD patients showed a significant (p < 0.05) post-operative elevation in plasma IL-6, p55, p75, and PLA(2) levels, but no significant change in TNF-alpha, IL-8, IL-10 or haptoglobin levels. The AAA patients had a significant post-operative rise in IL-10 levels and a significant decrease in plasma haptoglobin levels, but no significant change of TNF-alpha, IL-6, IL-8, p55, p75, or PLA(2) concentrations. The lap chole patients demonstrated no significant change in any of these parameters. CONCLUSION: These data show that IL-6, IL-10, p55, and p75 are markers to measure the degree of inflammatory stress associated with abdominal operative procedures and demonstrate the relative lack of a cytokine response to laparoscopic cholecystectomy.

Adult↗

PubMed2006

Anti-inflammatory treatment with standardized human serum protein solution reduces local and systemic inflammatory response after hemorrhagic shock.

OBJECTIVE: Reperfusion after hemorrhagic shock leads to local and systemic inflammatory response. This study evaluates the effect of a short-term treatment with standardized human serum protein solution (SPS) on the local and systemic inflammatory response in the mesenteric microcirculation in the rat. METHODS: Spontaneously breathing animals underwent median laparotomy and exteriorization of an ileal loop for intravital microscopy of the mesenteric microcirculation. Volume-controlled hemorrhagic shock was set by arterial blood withdrawal (2.5 ml/100 g body weight for 60 min), followed by reperfusion for 4 h. SPS (n = 10) or saline 0.9% (controls, n = 10) was given intravenously as a continuous infusion for 30 min at the beginning of reperfusion ('pre-hospital'). This was followed in both groups by substitution of blood and normal saline to support blood pressure ('in-hospital'). Systemic hemodynamics, mesenteric microcirculation and arterial blood gases were monitored before, during and after shock, and for 4 h after initiation of reperfusion. RESULTS: SPS treatment markedly reduced leukocyte/endothelial interaction, and reduced the need for intravenous fluids compared to controls. For the entire observation period, blood pH was unchanged from baseline only in SPS-treated animals. The improvement of base excess and abdominal blood flow persisted for 2 h after SPS infusion. CONCLUSION: Short-term SPS treatment of hemorrhagic shock improved mesenteric microcirculation, arterial blood gases and global hemodynamics, and attenuated the inflammatory response to reperfusion. It may provide clinical benefit when applied at an early phase of reperfusion after hemorrhagic shock.

Animals↗

PubMed1990

Antiallergic and anti-inflammatory action of tioxamast in rats. II. Anti-inflammatory action in vivo.

Tioxamast is an antiallergic drug that inhibits anaphylaxis in various models in rats, and it inhibits the release and synthesis of certain mediators of inflammation [see Tarayre et al., this issue]. Here we report that the drug also has an anti-inflammatory effect in vivo in various nonimmunological models in rats. It reduces zymosan-induced inflammation in the paw and pleural cavity, starting at doses from 1.5625 to 3.125 mg/kg given intraperitoneally. In pleurisy, tioxamast lowers the concentration of leukotriene B4 (LTB4) in the exudate, at doses from 50 mg/kg i.p. Also, at doses from 12.5 mg/kg i.p., the compound reduced PAF-acether-induced pleurisy and the concentrations of LTB4 and peptidoleukotrienes in the exudate. An anti-inflammatory action against carrageenin-induced edema of the paw was seen only at doses of 50 mg/kg i.p. or more. The anti-inflammatory and antiallergic effect of tioxamast makes it a potentially useful drug in the treatment of allergies in humans.

Animals↗

PubMed2001

The importance of balanced pro-inflammatory and anti-inflammatory mechanisms in diffuse lung disease.

The lung responds to a variety of insults in a remarkably consistent fashion but with inconsistent outcomes that vary from complete resolution and return to normal to the destruction of normal architecture and progressive fibrosis. Increasing evidence indicates that diffuse lung disease results from an imbalance between the pro-inflammatory and anti-inflammatory mechanisms, with a persistent imbalance that favors pro-inflammatory mediators dictating the development of chronic diffuse lung disease. This review focuses on the mediators that influence this imbalance.

Anti-Inflammatory Agents↗

PubMed1994

Anti-inflammatory effects of etodolac: comparison with other non-steroidal anti-inflammatory drugs.

The anti-inflammatory effects of etodolac (Eto) were compared with those of 6 other anti-inflammatory drugs: indomethacin (Ind), diclofenac Na (Dic), piroxicam (Pir), naproxen (Nap), ketoprofen (Ket) and aspirin (Asp). Eto inhibited carrageenin-induced edema in rats, adjuvant-induced arthritis in rats, acetic acid-induced writhing in mice and brewer's yeast-induced hyperalgesia and fever in rats. In the adjuvant arthritis test, the ED30 value (1.88 mg/kg) on day 3 and ED50 values (adjuvant-injected paw: 1.18 mg/kg and non-injected paw: 0.96 mg/kg) on day 18 for Eto were comparable to those for Dic (2.16, 1.72 and 1.28) when given prophylactically and the ED50 values for Eto (adjuvant-injected paw: 1.61 and non-injected paw: 1.20 mg/kg) were comparable to those for Ket (1.24 and 1.22) when used therapeutically. The analgesic activity of Eto (ED50 value: 3.67 mg/kg) in the acetic acid-induced writhing test was greater than that of Nap (9.83) or Asp (31.6) and less than that of Ind (0.71), Dic (1.54), Pir (0.92) or Ket (1.34). In the antipyretic test, the minimum effective dose (MED: 1 mg/kg) for Eto was comparable to that for Ind (1.0), Nap (1.0) or Ket (1.0). Eto was less potent in inhibiting carrageenin-induced edema (ED30 value: 6.99 mg/kg) and inflammatory pain (ED50 value: 9.24 mg/kg) than the other drugs (Ind: 2.32 and 3.47, Dic: 0.69 and 3.80, Pir: 1.31 and 1.94, Nap: 1.83 and 2.78, Ket: 1.12 and 0.63), except for Asp (167 and 51.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed2004

Anti-inflammatory effect of Semecarpus anacardium Linn. Nut extract in acute and chronic inflammatory conditions.

The article relates to investigation of the anti-inflammatory effects of Semecarpus anacardium LINN. nut extract (SA), and also an anti-inflammatory drug, indomethacin, on carrageenan-induced paw edema and cotton pellet granuloma tests for their effects on acute and chronic phases of inflammation, respectively. The effect of SA on developing and developed adjuvant arthritis was also evaluated. SA significantly decreased the carrageenan-induced paw edema and cotton pellet granuloma. Indomethacin also decreased the acute and chronic phases of inflammation. SA decreased the adjuvant induced (arthritis) paw edema after the treatment, in both developing and developed adjuvant arthritis. These results indicate that the potent anti-inflammatory effect and therapeutic efficacy of Semecarpus anacardium LINN. nut extract against all phases of inflammation, is comparable to that of indomethacin.

Acute Disease↗

PubMed1987

[Anti-inflammatory, analgesic and anti-pyretic activities of a new anti-inflammatory compound, 2-[4-(3-methyl-2-butenyl)phenyl] propionic acid (TA), in experimental animals].

Anti-inflammatory, analgesic and anti-pyretic activities of orally administered TA were investigated in experimental animals. Against acetic acid-induced vascular permeability in mice, carrageenin-induced hind paw edema in rats and ultra-violet ray-induced erythema in guinea pigs, TA produced a dose related inhibition at doses of 40-160 mg/kg, 10-40 mg/kg and 10-40 mg/kg, respectively. TA produced no inhibition against histamine-induced vascular permeability even at a dose of 200 mg/kg in rats. Cotton pellet-induced granuloma and adjuvant-induced arthritis in rats were significantly inhibited by repeated administration of TA at a dose of 50 mg/kg/day for 6 days and 25 mg/kg/day for 6 days, respectively. TA showed a dose related analgesic effect at a dose of 50-200 mg/kg in acetic acid writhing, Randall-Selitto and adjuvant arthritic pain methods. A high dose of TA was needed to produce an analgesic effect in the pressure method using mice. TA produced an anti-pyretic effect against the pyrexia induced by yeast in rats. On the other hand, TA showed no effect against normal body temperature in rats. These results suggest that anti-inflammatory, analgesic and anti-pyretic activities of TA are generally a little weaker than those of ibuprofen, and the mode of action of TA is similar to that of a typical acidic non-steroidal anti-inflammatory drug such as ibuprofen, indomethacin or phenylbutazone. The ulcerogenic activity of TA was about 2 and 4 times weaker than that of ibuprofen in rats and mice, respectively. TA showed a protective effect against gastric necrosis induced by HCl.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1986

Pharmacological studies on proglumetacin maleate, a new non-steroidal anti-inflammatory drug (4). Mode of action on anti-inflammatory activity.

The possible mechanism of the anti-inflammatory activity of proglumetacin maleate (PGM), a new indomethacin (IND) derivative interacting with arachidonic acid (AA) metabolism, was investigated to elucidate the contributions of PGM itself and its two major metabolites, desproglumideproglumetacin maleate (DPP) and IND. PGM caused much less inhibition of PGE2 formation by sheep seminal vesicle microsomes (IC50 = 310 microM) and TXB2 formation by a washed rabbit platelet suspension (IC50 = 6.3 microM) than IND. DPP also caused less inhibition of cyclooxygenase than IND. Moreover, PGM had less effect on sodium arachidonate (SAA)-induced rat platelet aggregation ex vivo and AA-induced sudden death in rabbits than IND. These results show that PGM has anti-inflammatory activity after its conversion to the active metabolite IND. However, the inhibitory effects of PGM and DPP were as strong as that of IND on SAA- or collagen-induced rabbit platelet aggregation in vitro. These activities are considered to be associated with platelet membrane interaction. Moreover, unlike IND, PGM (IC50 = 1.5 microM) and DPP (IC50 = 16.3 microM) strongly inhibited 5-HETE formation by the cytosol of guinea pig polymorphonuclear leukocytes. This unique activity of PGM on 5-lipoxygenase may contribute to its anti-inflammatory activity.

Animals↗

PubMed2006

Experimental study of the action of COX-2 selective nonsteroidal anti-inflammatory drugs and traditional anti-inflammatory drugs in bone regeneration.

OBJECTIVE: The aim of this study is to compare the effects of traditional nonsteroidal anti-inflammatory drugs with nonsteroidal anti-inflammatory drugs that are selective cyclooxygenase-2 (COX-2) inhibitors in the process of bone regeneration in a rat model. MATERIALS AND METHODS: Forty-four Wistar strain rats were subjected to osteotomy of the right femur and randomly divided into 3 groups according to the drug to be given (diclofenac, rofecoxib, or placebo). Each group was divided into 2 subgroups according to the time to euthanasia after the surgery. The animals of Subgroup 1 were submitted to euthanasia 2 weeks after surgery, and those of Subgroup 2, underwent euthanasia 4 weeks after surgery. Radiographic examinations and bone callus histomorphometry were analyzed. RESULTS: No intergroup statistical difference was found in the bone callus area or in bone formation area 2 and 4 weeks after surgery. Intra-group analysis concerning the bone neoformation area inside the callus showed a significant difference within the diclofenac group, which presented less tissue. CONCLUSIONS: Fracture consolidation in Wistar rats occurs within less than 2 weeks, and the use of nonsteroidal anti-inflammatory drugs does not significantly influence this process.

Animals↗

PubMed2006

[The role of long pentraxin 3, a new inflammatory mediator in inflammatory responses].

Pentraxin 3 (PTX3) is suggested to play important roles in the innate resistance against pathogens, regulation of inflammatory reactions, and clearance of apoptotic cells. PTX3 is the first long pentraxin identified. Long pentraxin shares a C-terminal pentraxin domain with the classical short pentraxin (C-reactive protein, serum amyloid P), but holds an unrelated N-terminal domain that is unique to the long pentraxin. While the short pentraxin is produced only in the liver, PTX3 is made by diverse types of cells, prominently endothelial cells and macrophage, in response to inflammatory signals. Unlike the short pentraxin, the expression of PTX3 in multiple types of tissue cells implies a mechanism for local amplification of innate resistance at the site of infection and inflammation. PTX3 plasma levels are very low in normal subjects but are rapidly increased by inflammatory conditions resulting from a wide range of diseased states, from infection to autoimmune and degenerative disorders. Critically ill patients show elevated circulating levels of PTX3 which are determined by the severity of the disease. Clinical evidence has demonstrated that the elevated PTX3 levels might be a useful early and sensitive marker for severely ill patients. Further studies will definitely be needed to deepen our understanding of PTX3.

Acute-Phase Proteins↗

PubMed2003

A novel anti-inflammatory role for simvastatin in inflammatory arthritis.

3-Hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) exert favorable effects on lipoprotein metabolism, but may also possess anti-inflammatory properties. Therefore, we explored the activities of simvastatin, a lipophilic statin, in a Th1-driven model of murine inflammatory arthritis. We report in this study that simvastatin markedly inhibited not only developing but also clinically evident collagen-induced arthritis in doses that were unable to significantly alter cholesterol concentrations in vivo. Ex vivo analysis demonstrated significant suppression of collagen-specific Th1 humoral and cellular immune responses. Moreover, simvastatin reduced anti-CD3/anti-CD28 proliferation and IFN-gamma release from mononuclear cells derived from peripheral blood and synovial fluid. Proinflammatory cytokine production in vitro by T cell contact-activated macrophages was suppressed by simvastatin, suggesting that such observations have direct clinical relevance. These data clearly illustrate the therapeutic potential of statin-sensitive pathways in inflammatory arthritis.

Animals↗

PubMed1992

Effects of nonsteroidal anti-inflammatory drugs on endogenous gastrointestinal prostaglandins and therapeutic strategies for prevention and treatment of nonsteroidal anti-inflammatory drug-induced damage.

Although nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for pain relief and treatment of arthritis, they can induce gastric and duodenal ulcers and life-threatening complications. The mechanisms of their anti-inflammatory action and their gastroduodenal toxic effects are related, in part, to inhibition of prostaglandin synthesis. This review article discusses prostaglandins, their functions in the gastrointestinal tract, anti-inflammatory actions of NSAIDs, and mechanisms by which NSAIDs produce gastroduodenal ulcers. Also reviewed are risk factors associated with the development of NSAID-related ulcers and pharmacologic strategies for the prevention and treatment of NSAID-induced ulcers.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2005

Non-inflammatory joint pain in patients with inflammatory bowel disease is prevalent and has a significant impact on health related quality of life.

OBJECTIVE: To describe the prevalence and characteristics of non-inflammatory joint pain (NIJP) in patients with chronic inflammatory bowel disease (IBD) and its impact on patients' health related quality of life (HRQOL). METHODS: In a population based cohort, 521 patients (80%) were clinically investigated 6 years after onset of IBD. NIJP was defined as a history of joint pain during the last 3 months prior to examination and the absence of concomitant signs or symptoms of inflammatory or degenerative joint disease or chronic pain syndromes. HRQOL was registered by the generic Medical Outcome Study Short Form 36 (SF-36) and by the disease specific IBDQ. RESULTS: NIJP was reported by 85 (16%) patients and significantly more often in conjunction with Crohn's disease (CD, 22%) compared to ulcerative colitis (UC, 14%). The prevalence of NIJP was similar in men and women. No correlation with extension of intestinal disease, use of systemic medication, or frequency of surgery was found. NIJP exerted significant impact on HRQOL measured by SF-36 and IBDQ. CONCLUSIONS: NIJP occurs frequently in IBD and more often in CD than in UC. NIJP significantly alters HRQOL and should be taken into account in trials estimating outcome in IBD and in clinical practice by attending clinicians.

Adult↗

PubMed1990

Bromfenac, a new nonsteroidal anti-inflammatory drug: relationship between the anti-inflammatory and analgesic activity and plasma drug levels in rodents.

Bromfenac [2-amino-3-(4-bromobenzoyl)benzenacetic acid, sodium salt sesquihydrate] exhibited potent analgesic and anti-inflammatory activity in mice and rats. In a mouse model of pain (acetylcholine abdominal constriction), bromfenac showed a rapid onset of activity (20 min) that persisted for at least 4 hr. In a rat model of inflammation (carrageenan foot edema), a single oral dose of bromfenac, 0.316 mg/kg, produced significant anti-inflammatory activity up to 24 hr after dosing. Bromfenac was readily absorbed after oral administration, peak plasma levels being achieved at the earliest time tested: 20 min in the mouse and 30 min in the rat. The plasma half-life of bromfenac in rats is less than 4 hr. Since the anti-inflammatory activity persisted for 20 to 24 hr in spite of its short plasma half-life, it appears that there is no direct correlation between duration of activity and plasma drug level.

Analgesia↗

PubMedDate not supplied

[Determination of endotoxin in inflammatory rheumatic diseases--the effect of nonsteroidal anti-inflammatory agents on intestinal permeability].

We measured the amount of plasma endotoxin in 95 patients with inflammatory rheumatic diseases (42 with ankylosing spondylitis; 12 with possible ankylosing spondylitis; 41 with rheumatoid arthritis) and in 16 patients with Crohn's disease with a quantitative Limulus assay. Significantly increased mean values were found in inflammatory rheumatic diseases and in Crohn's disease. Between 31% and 50% of the patients had endotoxin values higher than 10 pg/ml--none of the controls had such values. Patients on regular treatment with NSAIDS had higher amounts of endotoxin again. From our results we discuss an intestinal involvement in inflammatory rheumatic diseases. An inflammation of the gut with an increased permeability seems to be responsible for the raised plasma endotoxin levels compared to healthy controls. NSAIDs probably contribute to the increased permeability of the gut.

Adult↗

PubMed1982

[Evaluation of nonsteroidal anti-inflammatory drugs (NSAID) intended for use as topical anti-inflammatory drugs].

A procedure which can serve as a possible basis for the laboratory study of the topical effect of NSAID was investigated in rats or guinea pigs. The effect of NSAID was greatly influenced by physical characteristics of the preparation such as drug particle size, solubility, ointment base and concentration of drug. Moreover, it was also found to be affected by many technical factors such as animal fixation, drug application times and methods (rubbing times or occlusive dressing technique) and amounts applied which play an important role in topical preparation. The topical application of NSAID ointment (1% of indomethacin, ketoprofen or diclofenac sodium) markedly inhibited the paw edema by carrageenin in rats. The inhibitory activity was the same as that of steroidal ointment (0.12% betamethasone 17-valerate or 0.05% fluocinonide), but was less than that by oral administration of these NSAID. Also, the NSAID ointment obviously inhibited the ultraviolet erythema in guinea pigs and the swelling in the hind feet of adjuvant arthritic rats. The inhibitory activities of NSAID ointments on these inflammatory responses were almost the same as those obtained by oral administration of such NSAID and more potent than those of steroidal ointments. Furthermore, NSAID ointments increased the pain threshold in the inflamed foot as determined by the method of Randall and Selitto. The analgesic activity of NSAID ointment was more potent than that of steroidal ointment, but less than that of NSAID administered orally. On the other hand, neither the systemic effects such as decrease in weight of the adrenals and thymus which were noted when steroidal ointment was used, nor the gastrointestinal lesions which were found by oral administration of NSAID, were recognized in rats in which NSAID ointment was applied topically. The anti-inflammatory effects of NSAID ointment correlated well with the drug concentration at the site of inflammation. These findings suggest that NSAID ointment has a clinical use in the treatment of inflammatory diseases.

Administration, Topical↗

PubMed1997

Activin A: a novel player and inflammatory marker in inflammatory bowel disease?

Recently, we demonstrated a strong induction of activin expression after cutaneous injury. We speculated, therefore, that activin may be overexpressed during inflammatory processes in other tissues characterized by mesenchymal/epithelial structure. Herein, we show a strikingly increased expression of the activin beta A-subunit in surgical specimens from the gut of patients suffering from ulcerative colitis and Crohn's disease, whereas no activin beta A mRNA could be detected in the normal human digestive tract. The levels of activin beta A expression showed an outstanding correlation with the degree of inflammation as assessed by histologic analysis of adjacent tissue and expression analysis of the proinflammatory cytokine interleukin-1 beta. In situ hybridization studies revealed the highest levels of activin mRNA in the mucosa and submucosa of highly inflamed areas, particularly where the intestinal epithelium was damaged, but not in control tissue. In contrast, activin beta B mRNA levels in most specimens from inflamed areas were only slightly higher compared to control tissue. The strong overexpression of activin beta A in inflammatory bowel disease suggests a novel and important role of this growth and differentiation factor during inflammatory processes of the gut.

Activins↗

PubMed1997

Assessment of inflammatory cytokines, nitrate/nitrite, type II phospholipase A2, and soluble adhesion molecules in systemic inflammatory response syndrome.

Plasma endotoxin levels, nitrate/nitrite (NOx), type II phospholipase A2 (PLA2), soluble adhesion molecules, and inflammatory cytokines were measured in 34 patients with systemic inflammatory response syndrome (SIRS). Significant correlations were found between NOx values, PLA2 values, soluble adhesion molecules, and inflammatory cytokines, suggesting the possibility that these factors were deeply affected each other. When the 34 SIRS patients were divided into the group with sepsis (n = 20) and with the group with trauma without documented infection (n = 14), despite the fact that the difference in APACHE II scores was not significant, all of the factors except endotoxin were significantly higher in the sepsis group than in the trauma group, and the outcome was death in 4 of the 14 patients in the trauma group (28.6%), as opposed to 14 of the 20 patients in the sepsis group (70.0%). The mediator values measured in this study seemed to reflect the difference in the severity of the patients' disease and their outcome.

Adult↗