Anti Inflammatory Thesis

Anti Inflammatory Thesis-70
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.

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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 [3].

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 [4], 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 [13]. 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 [16].


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