Background: Prostaglandin E2 (PGE2) plays key physiological roles within the body’s organs and the systemic
environment. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the biosynthesis of PGE2, which can lead to global
PGE2 deficiency, resulting in serious side effects in the gastrointestinal, renal and other systems. In contrast, various pyridine
derivatives have been found to increase endogenous PGE2 levels within multiple organs and the systemic environment.
We hypothesised that the use of pyridine derivatives (nicotinic acid, nicotine, niceritrol, nicotinyl alcohol, pyridinol
carbamate, pyridoxine hydrochloride and pyridostigmine bromide) can recover PGE2 levels during NSAID treatment.
Methods: Reassessment of experimental data on PGE2 levels in NSAIDs and pyridine derivatives treatment, and in controls
from previously published, independent studies. Results: Overall, in all our investigations P values for unpaired or
pair-wise comparisons were not statistically significant. Conclusions: We demonstrated that using pyridine derivatives
along with NSAIDs, such as nonselective cyclooxygenase (COX) and selective COX-2 inhibitors, does not reduce endogenous
PGE2 expression to below basal levels. This finding is based on both in vitro studies using animal and human
tissues and in vivo studies performed with healthy volunteers. Using pyridine derivatives to correct a PGE2 deficiency during
NSAID treatment is a novel method that we propose can offer a valuable, cost-effective therapeutic approach to preventing
and treating the side effects of NSAIDs.
Keywords: Anti-inflammatory agents, drug development, drug interactions, drug side effects, non-steroidal anti-inflammatory
drugs, prostaglandin E2, pyridine derivatives.
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