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PubMed2005

Pretreatment of acetylsalicylic acid promotes tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by down-regulating BCL-2 gene expression.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been shown to be selective in the induction of apoptosis in cancer cells with minimal toxicity to normal tissues. However, not all cancers are sensitive to TRAIL-mediated apoptosis. Thus, TRAIL-resistant cancer cells must be sensitized first to become responsive to TRAIL. In this study, we observed that pretreatment by acetylsalicylic acid (ASA) augmented TRAIL-induced apoptotic death in human prostate adenocarcinoma LNCaP and human colorectal carcinoma CX-1 cells. Western blot analysis showed that pretreatment of ASA followed by TRAIL treatment activated caspases (8, 9, and 3) and cleaved poly(ADP-ribose) polymerase, the hallmark feature of apoptosis. Most interestingly, at least 12 h of pretreatment with ASA was prerequisite for promoting TRAIL-induced apoptosis and was related to down-regulation of BCL-2. Biochemical analysis revealed that ASA inhibited NF-kappaB activity, which is known to regulate BCL-2 gene expression, by dephosphorylating IkappaB-alpha and inhibiting IKKbeta activity but not by affecting the HER-2/neu phosphatidylinositol 3-kinase-Akt signal pathway. Overexpression of BCL-2 suppressed the promotive effect of ASA on TRAIL-induced apoptosis and changes in mitochondrial membrane potential. Taken together, our studies suggested that ASA-promoted TRAIL cytotoxicity is mediated through down-regulating BCL-2 and by decreasing mitochondrial membrane potential.

Apoptosis↗
PubMed1978

Evaluation of effect of acetylsalicylic acid using electrical stimulation on the forefinger of healthy volunteers.

1 In order to determine the optimal level of electrical stimulation, the degree of pain sensitivity produced by electrical stimulation on the volar side of terminal phalange of the right forefinger was studied in 22 male and female volunteers between the ages of 20 and 27 years. 2 A stimulation frequency of 400 Hz, width of 0.1 ms and electrical potential of 55 V was found to be optimal for study fo analgesics. 3 The effect of acetylsalicylic acid was studied in 40 healthy male volunteers between the ages of 20 and 25 years. Electrical stimulation was applied for 5 s under a single-blind method at a frequency of 400 Hz, width of 0.1 ms and electrical potential of 25, 35 and 55 V. Placebo, 250 mg, 500 mg and 1 000 mg of acetylsalicyclic acid were administered orally under double-blind method conditions. 4 As a result of this study, it was found that acetslsalicylic acid in a dose of 500 and 1 000 mg, was effective in relieving pain with statistically significant differences from a placebo.

Adult↗
PubMed2006

Fracture risk associated with use of nonsteroidal anti-inflammatory drugs, acetylsalicylic acid, and acetaminophen and the effects of rheumatoid arthritis and osteoarthritis.

We studied the effects of various nonmorphine pain medications as well as rheumatoid arthritis and osteoarthritis on fracture risk in a nationwide case-control study. Cases were all subjects with any fracture sustained during the year 2000 (n = 124,655) in Denmark. For each case, three controls (n = 373,962) matched on age and gender were randomly drawn from the background population. The primary exposure variables were use of acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), or acetylsalicylic acid (ASA). Adjustments were made for several confounders. The effect of dose was examined by stratifying for cumulated dose (defined daily dose, DDD). For acetaminophen, a small increase in overall fracture risk was observed with use within the last year (odds ratio [OR] = 1.45, 95% confidence interval [CI] 1.41-1.49). For ASA, no increase in overall fracture risk was present with recent use. Significant heterogeneity was present for the NSAIDs; e.g., ibuprofen was associated with an increased overall fracture risk (OR = 2.09, 95% CI 2.00-2.18 for <20 DDD), while celecoxib was not (OR = 0.76, 95% CI 0.51-1.13 for <20 DDD, 2P < 0.01 for comparison). Osteoarthritis was associated with a decreased risk of any fracture if the diagnosis had been made more than 1 year ago (OR = 0.70, 95% CI 0.67-0.72). Rheumatoid arthritis was associated with an increase in overall fracture risk if the diagnosis had been made within the last year (OR = 1.86, 95% CI 1.68-2.07). Weak analgesics may be associated with fracture risk in a varying way. The effects in most cases were small. Falls may be one reason for the increase in fracture risk with some NSAIDs.

Acetaminophen↗
PubMed1982

Effect of acetylsalicylic acid on platelet aggregation and thromboxane B2 production in flowing aortic blood in the rat studied with a filter loop technique.

A method of measuring in vivo platelet function using a filter loop technique has been used to study platelet aggregation in response to Adenosine Diphosphate (ADP) and Sodium Arachidonate infusion in flowing aortic blood in the rat. ADP infusion produced reversible platelet aggregation in vivo with no change in thromboxane B2 (TXB2) levels whereas sodium arachidonate infusion resulted in virtually irreversible aggregation with a rise in TXB2 levels. Oral Acetylsalicylic Acid (ASA) in doses of 1-100 mg/kg had no effect on ADP induced aggregation but prevented platelet aggregation in vivo induced by sodium arachidonate and the concomitant rise in TXB2 levels.

Adenosine Diphosphate↗
PubMed1981

Regulation of 25-hydroxy-vitamin D-1 alpha-hydroxylase in chick isolated renal tubules: effects of prostaglandin E2, frusemide and acetylsalicylic acid.

1. Isolated renal tubules were prepared from vitamin D-deficient chicks. The effects of added prostaglandin E2 (PGE2) and agents which modify prostaglandin metabolism on the metabolism of 25-hydroxy-vitamin D3 were studied. 2. Frusemide (0.1 mmol/l) raised the prostaglandin E (PGE) content of the tubule incubation medium; it significantly increased 1,25-dihydroxy-vitamin D3 [1,25-(OH)2D3] production from 25-hydroxy-vitamin D3 [25-(OH)D3] and significantly inhibited the net production of 24,25-dihydroxy-vitamin D3 [24,25-(OH)2D3]. 3. Acetylsalicylic acid (aspirin; 0.1 mmol/l) decreased the PGE content of the tubule incubation medium and significantly inhibited 1,25-(OH)2D3 production. 4. In the presence of 1,25-(OH)2D3, 4 h exposure of tubules from vitamin D-deficient chicks to concentrations of PGE2 between 2.8 X 10(-6) and 2.8 X 10(-8) mol/l significantly enhanced 1,25-(OH)2D3 production. 5. It is concluded that, in view of the effects of modulation of endogenous prostaglandin levels by frusemide in aspirin, and the stimulatory effect of exogenous PGE2, prostaglandins should be considered potential regulators of the renal 25-hydroxy-vitamin D-1 alpha-hydroxylase [25-(OH)D-1 alpha-hydroxylase] enzyme.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed2005

Acetylsalicylic acid improves lipid-induced insulin resistance in healthy men.

CONTEXT AND OBJECTIVE: Insulin resistance is a central feature of type 2 diabetes. Salicylates prevent lipid-induced insulin resistance in rodents by interrupting inflammatory pathways. We therefore investigated whether salicylates reduce lipid-induced insulin resistance in humans by affecting inflammatory pathways as reflected by serum adipocytokines. PARTICIPANTS AND INTERVENTION: Ten healthy men were included in a crossover intervention study. Four euglycemic-hyperinsulinemic clamps were performed, one without pretreatment, one with prior 2-h lipid infusion, one after pretreatment with 4 g acetylsalicylic acid (ASA), and one with ASA pretreatment and prior lipid infusion. MAIN OUTCOME MEASURE: Lipid-induced insulin resistance was quantified by the euglycemic-hyperinsulinemic clamp technique running at least 2 h. Repeated-measures ANOVA on two factors was used for comparison, and results were Bonferroni adjusted for multiple measurements. ASA effects on serum adipocytokines were addressed by comparing the areas under the curves. RESULTS: Glucose infusion rate (M value) of the control clamp without pretreatment was 6.3 (+/- 0.6) mg/kg.min. ASA pretreatment did not change glucose infusion rates (P = 0.6). Lipid infusion significantly decreased the M value to 4.1 (+/- 0.6) mg/kg.min (P = 0.008). After ASA pretreatment and lipid infusion, the M value was 4.8 (+/- 0.7) mg/kg.min and was significantly improved, compared with the lipid-only clamp (P = 0.036 after Bonferroni's adjustment). General biomarkers of inflammatory processes (IL-6, C-reactive protein), the insulin-sensitizing mediator adiponectin, and circulating adiponectin oligomers were unchanged by ASA pretreatment. CONCLUSIONS: ASA pretreatment attenuated lipid-induced insulin resistance in healthy humans. This acute insulin-sensitizing effect of ASA was unrelated to changes of circulating inflammatory markers.

Adiponectin↗
PubMed1986

Endotoxin protection against oxygen toxicity and its reversal by acetylsalicylic acid.

This study investigated the involvement of substances derived from arachidonic acid in the mechanism of endotoxin's protective action against pulmonary oxygen toxicity. Eighty-three percent of rats treated with a small dose of endotoxin (1 mg/kg) survived exposure to over 95% oxygen for 7 days. In contrast, all control rats exposed to the same oxygen concentration died within 3 days. When the endotoxin-treated rats were also treated with the soluble lysine salt of acetylsalicylic acid (100 mg/kg), 7-day survival decreased to 25%. This suggests that prostaglandin metabolism may play an important role in the protective action of endotoxin during hyperoxia.

Animals↗
PubMed2003

Influence of acetylsalicylic acid and ketoprofen on canine thyroid function tests.

Many factors including drugs can influence thyroid function in humans, rats and dogs. Studies in humans report significant effects of non-steroidal anti-inflammatory agents (NSAIDs) on thyroid function tests, which can lead to misinterpretation of the results and inappropriate therapeutic decisions. As NSAIDs are used more and more frequently in dogs, it is important to know to what extent they can influence results. Eighteen spayed female beagle dogs were randomly assigned to three treatment sequences in a 3 x 3 crossover study design with treatments consisting of acetylsalicylic acid (ASA) (25 mg/kg BW q 12 h), ketoprofen (Keto) (1 mg/kg BW q 24 h) or placebo administered for a 1-week period with a 3-week washout period between treatment periods. Blood samples for determination of total thyroxine (TT4), free thyroxine (FT4), total triiodothyronine (TT3), thyrotropin (TSH), reverse triiodothyronine (rT3), Keto and ASA concentrations were taken during each treatment period on days 0, 1, 3 and 7. During the washout period samples were taken weekly. A significant decrease in TT4 was observed as soon as 24 h after ASA administration, whereas the decrease in TT3 was less pronounced and differed significantly from the placebo only after 1 week of administration. No significant effects were found for free T4 and TSH with ASA administration. No significant effects on thyroid results were found following Keto administration. The results indicate that TT4 can be markedly decreased by ASA therapy and until the results of further studies are available, thyroid function test results should be interpreted cautiously in dogs on NSAIDs therapy.

Animals↗
PubMed1999

Topical acetylsalicylic acid versus lidocaine for postherpetic neuralgia: results of a double-blind comparative clinical trial.

A double-blind comparative clinical trial was performed with topical aspirin versus lidocaine for the treatment of 40 patients with postherpetic neuralgia. The percentage improvement following topical aspirin application was 72.2 +/- 19.9 S.D., while with lidocaine it was 72.8 +/- 25.3 S.D. These results suggest that the effect of topical treatment with aspirin is as good as that with lidocaine, since there was no significant difference (P = 0.778) between the two drugs in respect of pain reduction and accordingly the topical application of acetylsalicylic acid can be equally recommended.

Adult↗
PubMed2006

Acetylsalicylic acid enhances antiproliferative effects of the EGFR inhibitor gefitinib in the absence of activating mutations in gastric cancer.

The epidermal growth factor receptor (EGFR) is highly expressed in gastric cancer indicating its suitability as a target for receptor tyrosine kinase (RTK) inhibitors. In the current study we explored the role of EGFR and its potential use as a therapeutic target in gastric cancer. First we analyzed 66 gastric cancer samples of Asian and Caucasian patients for the presence of EGFR mutations. No activating EGFR mutations were found and gefitinib alone was only weakly effective in gastric cancer cell lines. However, acetylsalicylic acid (ASA) significantly enhanced the inhibitory effects of gefitinib indicating synergistic action. Whole genome expression profiling indicated significant regulation of 120 genes in the case of co-administration of gefitinib and ASA (32 induced, 88 repressed) in gastric adenocarcinoma cells. Further analyses indicated that several important signalling pathways were effectively inhibited by simultaneous exposure to gefitinib and ASA. Our findings indicate that although gastric cancer does not seem to harbour mutations which render the cancer cells constitutively susceptible to gefitinib, the co-administration of ASA can strengthen RTK inhibitor activity in adenocarcinoma cells by EGFR activation. This is the first report of effective modulation of EGFR-inhibition activity in cancer.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Catheter thrombosis during primary percutaneous coronary intervention for acute ST elevation myocardial infarction despite subcutaneous low-molecular-weight heparin, acetylsalicylic acid, clopidogrel and abciximab pretreatment.

BACKGROUND: Subcutaneous enoxaparin is increasingly employed as the antithrombin of choice in non-ST elevation myocardial infarction and in conjunction with various fibrinolytic regimens in acute ST elevation myocardial infarction (STEMI). Few data exist describing the use of subcutaneous or intravenous enoxaparin as an anticoagulant in the highly thrombotic setting of primary percutaneous coronary intervention (PCI) for STEMI. METHODS: The Which Early ST Elevation Therapy (WEST) study compared fibrinolysis (with and without early cardiac catheterization) with primary PCI in a setting that expedited both strategies on first medical contact. Patients assigned primary PCI are administered acetylsalicylic acid 325 mg, clopidogrel 300 mg and subcutaneous enoxaparin 1 mg/kg before transport to a PCI centre. Of 36 initial patients treated with primary PCI, three patients had procedures that were complicated by extensive thrombosis within coronary catheters and on PCI equipment. RESULTS: Index cases were men aged 43 to 68 years who presented with confirmed STEMI and angiographically proven acute total or subtotal occlusion of a major epicardial coronary segment. During PCI, performed 76 min to 102 min following enoxaparin administration, a clot developed within the guide catheter or on the coronary guidewires and balloon catheter shafts, thus necessitating the replacement of all PCI equipment. In one case, there was evidence of continued intracoronary clot propagation and embolization. CONCLUSION: A single, conventional, weight-adjusted dose of subcutaneous enoxaparin before expedited primary PCI for STEMI may not provide a reliable antithrombotic effect. Supplementary intravenous enoxaparin is now strongly recommended within the WEST study, and a substudy evaluating pre- and postprocedural antifactor Xa activity has been initiated.

Abciximab↗
PubMed2000

[Use of platelet function analyzer PFA-100 and whole blood aggregometry to monitor blood platelet sensitivity to acetylsalicylic acid (aspirin). Is it possible to reliably monitor antiplatelet treatment using routine laboratory diagnostic methods?].

Introduction of the antiplatelet agents of new generations and the occurrence of the phenomenon of "aspirin-resistance" triggered the search for better, simpler and more reliable routine diagnostic methods to monitor platelet reactivity. Our objective was to evaluate the usefulness and reliability of two simple methods: platelet function analyzer (PFA-100) and whole blood platelet aggregometry for monitoring of platelet function in 18 healthy blood donors and 35 patients with ischaemic heart disease (IHD) subjected to small doses/75 mg and 150 mg a day) of acetylsalicylic acid (aspirin). In 50% of healthy blood donors the intake of 75 mg ASA a day resulted in the prolongation of PFA-100 collagen/epinephrine closure time (CEPI = (relevant to reduced platelet reactivity) of over 150 s, whereas 75% donors responded to 150 mg ASA-. Otherwise, the daily dose of 150 mg ASA resulted in a prolonged CEPI merely in 23% of in IHD patients. At both doses ASA completely inhibited the arachidonic acid-induced whole blood platelet aggregation in all healthy donors and in all but 3 IHD patients. Collagen-induced platelet aggregation was only negligibly affected by either dose of ASA. Our results point that the simultaneous monitoring of the PFA-100 collagen/epinephrine closure time and whole blood platelet aggregometry (Chrono-Log) enables to reliably evaluate the inhibition of platelet function by ASA and discriminate the partial or complete platelet insensitivity to aspirin. The phenomenon of more frequent platelet aspirin-resistance in IHD patients requires to be verified in randomised clinical prospective studies.

Adult↗
PubMed1982

Plasma carboxypeptidase activity and intolerance to acetylsalicylic acid unimpaired CP-N activity in ASA-intolerant individuals.

Carboxypeptidase N (EC 3.4.17.3, arginine carboxypeptidase, kininase, anaphylatoxin inactivator) activity was determined in human sera with the method of Erdös by differential spectrometry at 254 nm and 37 degrees C, using hippuryl-L-argininic acid (HLAa) as a substrate. Day-to-day imprecision (CV) of the assay was 6.5%. The reference value, as determined in 15 healthy blood donors, was 3,082 +/- 432 IU/1. The mean value in a pool of sera from 12 healthy pregnant women, 4,500 +/- 294 IU/1, was higher in accordance with earlier findings by Erdös et al. Sera from 53 patients with chronic asthma or chronic urticaria, without known acetylsalicylic acid (ASA) intolerance, gave the mean value of 3,583 +/- 768 IU/1, and those from 17 patients with chronic asthma or chronic urticaria and ASA intolerance 3,379 +/- 575 IU/1. Thus, the carboxypeptidase-N activity in the blood of ASA-intolerant asthmatics and urticaria patients was unimpaired. A 16-year-old boy with asthma and without ASA intolerance showed an unusually low value of 2,056 IU/1.

Aspirin↗
PubMed1988

The effect of fosfosal and acetylsalicylic acid on leukocyte migration and PGE2 concentration in experimentally induced acute inflammation.

The effect of fosfosal, a non-acetylated salicylic acid derivative, on the content of prostaglandin E2 (PGE2) and the migration of polymorphonuclear leukocytes in inflammatory exudates induced by s.c. implantation of 0.5% carrageenan soaked sponges in rats has been determined. Fosfosal, which does not inhibit PG synthesis in vitro, is capable of reducing, in a dose-dependent manner, the PGE2 content of the exudates, with a maximum reduction of 50-60% at a total dose of 100 mg/kg i.p. Acetylsalicylic acid was slightly more potent (68% reduction, 2 x 50 mg/kg i.p.). Six hours after fosfosal administration, salicylic acid, the principal metabolite of fosfosal, accumulated in the exudates at concentrations of about 100 micrograms/ml. These concentrations were sufficient to inhibit PG synthetase activity in vitro. Neither fosfosal nor acetylsalicyclic acid affected polymorphonuclear leukocyte migration at doses which significantly reduced the concentrations of PGE2. Indomethacin, used as reference, reduced leukocyte migration by 28 and 45% at a dose of 1 and 10 mg/kg i.p. respectively. The results indicate that fosfosal, in spite of its lack of effect on PG biosynthesis in vitro, exerts an effect on the inflammatory locus in vivo which may account, at least in part, for its anti-inflammatory activity. Moreover, our results confirm that the inhibition of PG synthesis and leukocyte migration are mediated by different mechanisms.

Animals↗
PubMed2006

The platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment.

INTRODUCTION: Addition of clopidogrel to patients treated with ASA has been shown to decrease the incidence of in-stent thrombosis after percutaneous coronary interventions. However, it has also been reported that up to 30% of patients do not achieve adequate platelet inhibition from standard dosages of ASA and clopidogrel. There is a demand for reliable methods to measure the individual platelet inhibiting effect of this combination therapy. MATERIALS AND METHODS: The primary aim of the present investigation was to compare three methods for evaluation of the platelet inhibiting effect of a clopidogrel bolus dose in patients on long-term acetylsalicylic acid treatment. Thirty patients presenting for coronary angiography/PCI were included. Two patients were excluded due to technical problems. All patients were on 75-100 mg ASA/day for at least 8 days. Blood samples were analysed before and 16 h after a 300 mg clopidogrel bolus dose. The platelet inhibiting effect was measured with (1) Whole blood flow cytometry (17 patients); (2) a bed-side test, Platelet Mapping assay for the thrombelastograph (28 patients); and (3) PFA (Platelet function analyser) -100 (26 patients). RESULTS: With flow cytometry, the percentage of platelets expressing P-selectin (p=0.03) on their surface decreased significantly after the bolus dose of clopidogrel. There was also a reduction of platelets binding fibrinogen when stimulated with ADP. A significantly (p=0.002) increased platelet inhibition could also be demonstrated with Platelet Mapping. PFA-100 could not measure any significant platelet inhibiting effect of clopidogrel. CONCLUSION: A significant platelet inhibition could be demonstrated with flow cytometry and the Platelet Mapping assay, but not with PFA-100. However, levels of response for the individual patient with these three methods were inconsistent. Further studies are needed to evaluate how the results correlate to the clinical risk of thrombosis and bleeding.

Aged↗
PubMed1976

[Effect of acetylsalicylic acid on immunologically induced morphologic changes after experimental lung transplantation (light and electron microscopic study)].

In 3 comparing series the behavior of platelets after experimental lung transplantation was examined in 33 dogs. After allogenic transplantations (21 animals) the ultrastructural findings were pathologic changes of the platelets, such as hyperaggregability with irreversible aggregation prevailing, as well as capillary wall alterations. X-rays showed considerable reduction of functioning parenchyma. Since these findings were absent in animals which underwent merely pulmonary re-implantation (4 animals) and can be considered a controll group, the authors conclude that these alterations are caused by mainly immunologic reactions. Acetylsalicylic acid given to animals with grafted lungs significantly inhibited is specific and certainly immuneinduced pathologic development. Absolutely necessary, therefore, appears the application of such aggregation inhibitor as additional treatment in lung transplantations.

Animals↗
PubMed2000

Microcrystalline cellulose from soybean husk: effects of solvent treatments on its properties as acetylsalicylic acid carrier.

Microcrystalline cellulose (MCC) is a very important product in pharmaceutic, food, cosmetic and other industries. In this work, MCC was prepared from soybean husk, produced in large quantities in soybean oil processing industries. It was characterized through various techniques (scanning electron microscopy (SEM), infrared spectroscopy (FTIR), thermogravimetry analysis (TGA) and differential scanning calorimetry (DSC)) and compared with a commercial MCC. The results obtained show that the prepared sample has similar crystallinity and lower particle size than the commercial MCC. Both MCC samples were treated with organic solvents (chloroform, acetone, ethanol and ethyl ether), for structural modifications to be introduced, and used as acetylsalicylic acid (ASA) carrier. Pretreated MCC and MCC/ASA 1:1 mixtures were analyzed through FTIR and thermal analysis. The drug release was evaluated in buffer solution of pH 4.5 and in pure water, at 37 degrees C. The MCC pretreated with different solvents show different thermal properties and ASA release rates, each MCC showing a particular behavior.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Acetylsalicylic acid accelerates the antidepressant effect of fluoxetine in the chronic escape deficit model of depression.

Evidence has accumulated suggesting that major depression is associated with dysfunction of inflammatory mediators. Moreover, antidepressants show an anti-inflammatory action possibly related to their clinical efficacy. An improvement in psychiatric symptoms has been recently reported in patients treated with anti-inflammatory drugs for other indications. These data imply that inflammation may be involved in the pathogenesis of depression and that anti-inflammatory drugs may be used as an adjunctive therapy. The aim of the present study was to evaluate the behavioural effect of the co-administration of acetylsalicylic acid (ASA, 45 mg/kg or 22.5 mg/kg) and fluoxetine (FLX, 5 mg/kg) in the chronic escape deficit model of depression. The chronic escape deficit model is based on the modified reactivity of rats to external stimuli induced by exposure to unavoidable stress and allows evaluation of the capacity of a treatment to revert the condition of escape deficit. In this model, FLX alone needs to be administered for at least 3 weeks to revert this condition. Our results show that combined treatment of fluoxetine and ASA completely reverted the condition of escape deficit by as early as 7 days, the effect being already partially present after 4 days. The effect was maintained after 14 and 21 days of treatment. ASA alone was ineffective at any time tested and the effect of fluoxetine was significant only at 21 days. These results, together with clinical data from preliminary results, suggest that ASA might accelerate the onset of action of selective serotonin reuptake inhibitor antidepressants.

Animals↗