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In the present study, we show that ascorbic acid dose-dependently inhibitedinterleukin-1beta (IL-1beta)-mediated PGE2 synthesis in the human neuronal cellline, SK-N-SH. Furthermore, in combination with aspirin, ascorbic acidaugmented the inhibitory effect of aspirin on PGE2 synthesis. However, ascorbicacid had no synergistic effect along with other COX inhibitors (SC-58125 andindomethacin). The inhibition of IL-1beta-mediated PGE2 synthesis by ascorbicacid was not due to the inhibition of the expression of COX-2 or microsomalprostaglandin E synthase (mPGES-1). Rather, ascorbic acid dose-dependently(0.1-100 microM) produced a significant reduction in IL-1beta-mediatedproduction of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a reliableindicator of free radical formation, suggesting that the effects of ascorbicacid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenanceof the neuronal redox status since COX activity is known to be enhanced byoxidative stress. Our results provide in vitro evidence that theneuroprotective effects of ascorbic acid may depend, at least in part, on itsability to reduce neuronal COX-2 activity and PGE2 synthesis, owing to itsantioxidant properties. Further, these experiments suggest that a combinationof aspirin with ascorbic acid constitutes a novel approach to render COX-2 moresensitive to inhibition by aspirin, allowing an anti-inflammatory therapy withlower doses of aspirin, thereby avoiding the side effects of the usually highdose aspirin treatment.

Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production