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No increase in the concentrations of either NF-κB target was seen after treatment with TNF-α.Nitrate-nitrite assay results did not show significant differences between any groups ().Thus, therapeutic effects of SDG in microglia may be attributed to other mechanisms.
This observation led to the discovery of acetyl salicylic acid, the active component of aspirin, a major anti-inflammatory drug widely used in clinical practice, along with many other non-steroidal anti-inflammatory drugs (NSAIDs) in current use .
Non-steroidal anti-inflammatory drugs are commonly prescribed for treatment of pain and inflammatory conditions such as rheumatoid arthritis, osteoporosis and Alzheimer’s disease.
With a number of studies recognizing the various health benefits of SDG, few have focused on its potential anti-inflammatory effect and, specifically, its interaction with the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.
Thus, the aim of this study is to elucidate the interaction between SDG and NF-κB in microglial cells .
However, because many NSAIDs are associated with side effects such as gastrointestinal bleeding and suppressed function of the immune system , attention has shifted to alternative pharmacotherapies [5, 6].
Recent studies on Zingiber officinale, ginger, suggest that it might be as effective as some NSAIDs in the treatment of inflammation and related pain [7, 8].
The antioxidant activities of acetone extracts were determined by measuring the free radical scavenging activity and ferric reducing ability, respectively.
The anti-inflammatory activities of the extracts were determined by measuring the inhibitory effect of the extracts on the activities of the pro-inflammatory enzyme, lipoxygenase and inducible nitric oxide synthase.
Flavonoids are a group of polyphenols thought to inhibit the biosynthesis of prostaglandins, end-products in the COX and LOX pathways of immunologic responses . COX-1 and COX-2, with a recently described third isomeric-form, COX-3 that is selectively inhibited by acetaminophen and related compounds [14, 15].
The selective inhibition of COX-2 is more desirable because the inhibition of COX-1 in the gastric mucosa is associated with the undesirable effects of NSAIDs .