Zpol
Member
- Joined
- Apr 14, 2013
- Messages
- 929
- Age
- 45
Wondering whether to take aspirin or Ascorbic Acid, and wondering if taking high dose would be necessary; looks like taking a low dose of both would be best.
Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production
Effect of vitamin C-releasing acetylsalicylic acid on gastric mucosal damage before and after Helicobacter pylori eradication therapy
So, if I understand this correctly, and if the studies are legit (I only have access to the abstracts), then...
The AA would enhance the ASA COX-2 inhibition and reduction of prostaglandin production action, so less of the ASA would be needed and therefore less side effects, plus the ASA would balance the redox imbalance caused by the AA and the AA would apparently simultaneously reduce oxidative stress if it's too high due to a stressor (H-pylori treatment in this case).
Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production
"Inhibition of neuronal cyclooxygenase-2 (COX-2) and hence prostaglandin E2 (PGE2) synthesis by non-steroidal anti-inflammatory drugs has been suggested to protect neuronal cells in a variety of pathophysiological situations including Alzheimer’s disease and ischemic stroke. Ascorbic acid (vitamin C) has also been shown to protect cerebral tissue in a variety of experimental conditions, which has been attributed to its antioxidant capacity. In the present study, we show that ascorbic acid dose-dependently inhibited interleukin-1β (IL-1β)-mediated PGE2 synthesis in the human neuronal cell line, SK-N-SH. Furthermore, in combination with aspirin, ascorbic acid augmented the inhibitory effect of aspirin on PGE2 synthesis. However, ascorbic acid had no synergistic effect along with other COX inhibitors (SC-58125 and indomethacin). The inhibition of IL-1β-mediated PGE2 synthesis by ascorbic acid was not due to the inhibition of the expression of COX-2 or microsomal prostaglandin E synthase (mPGES-1). Rather, ascorbic acid dose-dependently (0.1-100 µM) produced a significant reduction in IL-1β-mediated production of 8-iso-prostaglandin F2α (8- iso-PGF2α), a reliable indicator of free radical formation, suggesting that the effects of ascorbic acid on COX-2-mediated PGE2 biosynthesis may be the result of the maintenance of the neuronal redox status since COX activity is known to be enhanced by oxidative stress. Our results provide in vitro evidence that the neuroprotective effects of ascorbic acid may depend, at least in part, on its ability to reduce neuronal COX-2 activity and PGE2 synthesis, owing to its antioxidant properties. Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment. "
Effect of vitamin C-releasing acetylsalicylic acid on gastric mucosal damage before and after Helicobacter pylori eradication therapy
"The interaction between Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid is still controversial. This study was designed to compare the effect of acetylsalicylic acid and vitamin C-releasing acetylsalicylic acid on the gastric mucosal damage and microbleeding before and after eradication of H. pylori in 10 young healthy volunteers. Acetylsalicylic acid induced significantly more gastric lesions and higher microbleeding than acetylsalicylic acid-vitamin C. After successful H. pylori eradication therapy, acetylsalicylic acid induced significantly higher mucosal lesions and microbleeding than before eradication. In contrast, after acetylsalicylic acid-vitamin C, gastric lesion index was significantly lower and eradication therapy failed to aggravate it. All H. pylori-positive subjects showed significant up-regulation of antioxidant enzyme (superoxide dismutase, catalase, glutathione peroxidase). Plain acetylsalicylic acid stronger than acetylsalicylic acid-vitamin C reduced gastric gene expression of these antioxidant enzymes. H. pylori eradication significantly decreased expression of these enzymes and this was further enhanced by plain acetylsalicylic acid, but not acetylsalicylic acid-vitamin C. Under plain acetylsalicylic acid therapy, the expression of proinflammatory cytokines was increased before and after eradication of H. pylori. We conclude that vitamin C combined with acetylsalicylic acid, unlike plain acetylsalicylic acid without vitamin C, protects gastric mucosa in man probably due the attenuation of oxidative stress and proinflammatory cytokines."
So, if I understand this correctly, and if the studies are legit (I only have access to the abstracts), then...
The AA would enhance the ASA COX-2 inhibition and reduction of prostaglandin production action, so less of the ASA would be needed and therefore less side effects, plus the ASA would balance the redox imbalance caused by the AA and the AA would apparently simultaneously reduce oxidative stress if it's too high due to a stressor (H-pylori treatment in this case).
