![]() This theory, however, has been challenged because of discrepancies in clinical efficacies of aspirin in the treatment of diseases such as rheumatic fever, gout, and rheumatoid arthritis, which require much higher doses of aspirin (4–8 g/day) than required to inhibit prostaglandin production (1 (), 3 ()). The most well accepted mechanism of action of aspirin is inhibition of prostaglandin biosynthesis (2 ()). The broad range of biological actions of aspirin have made it difficult to delineate its mechanisms of action. These drugs have an enormous range of effects, including reducing pain or fever, dissolving corns, inhibiting blood clotting, inducing peptic ulcers, and promoting uric acid loss and fluid retention by the kidneys (1 ()). These findings indicate that inhibition of iNOS expression and NO production may explain, in part, the beneficial effects of aspirin as an anti-inflammatory agent at therapeutic concentrations, whereas inhibition of de novo protein synthesis may possibly explain clinical and side effects of aspirin in the inflamed tissues and organs such as stomach and kidney that may accumulate high concentrations of aspirin.Īspirin and ALD are the most commonly indicated agents for treatment of inflammation. Aspirin at high concentrations of 10 and 20 mminhibited de novo protein synthesis as demonstrated by inhibition of methionine incorporation into total islet protein and by inhibition of rabbit reticulocyte expression by Brome mosaic virus mRNA, suggesting that inhibition of iNOS expression at these high concentrations of aspirin may be due to the impairment of the translational machinery. Aspirin (1–5 mm) did not affect insulin secretion at basal or glucose-stimulated conditions, whereas higher concentrations of aspirin (10–20 mm) significantly increased basal insulin secretion. The effects of aspirin on islet function were examined by measuring glucose-stimulated insulin secretion in the presence of various concentrations of aspirin. Therapeutic concentrations of aspirin (1–5 mm) that block NO production affected neither nuclear factor-κB activation nor inducible NO synthase (iNOS) mRNA transcription but potently inhibited iNOS protein expression by both RINm5F cells and rat islets. In this study, we examined the effects of aspirin on production of nitric oxide (NO), a proinflammatory mediator, and show that aspirin inhibits NO production by transformed pancreatic β cells (RINm5F) and rat islets in a concentration-dependent manner with an IC50 value of ∼3 mm. Mechanisms of action for these drugs, however, are not clearly understood. Louis, Missouri 63110Īspirin and aspirin-like drugs are the most commonly indicated agents for the treatment of inflammation. I think this is the science behind the "no aspirin" concept:Įffects of Aspirin on Nitric Oxide Formation and De Novo Protein Synthesis by RINm5F Cells and Rat Isletsĭepartment of Pathology, Washington University School of Medicine, St. ![]() cold or flu, ASA or at least some aspirin product such NSAIDS or tylenol. What do people take when they have a fever i.e. Hence, your body temp will be slightly elevated. Remember, with ephedra you get a thermogenic effect. I asked Dave P this a while back and he stated the same thing. ![]()
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