review article of anti-inflammatory effects of Boswellia. Boswellia inhibits 5-LOX and resultant leukotrienes. 3-actyl-11-keto-Beta-boswellic acid is the most potent inhibitor of 5-LOX. As it relates to disease states and symptoms, Boswellia reduces pain in OA and RA. Boswellia also shown to inhibit NF-kappa B: a potent nuclear transcription factor for inflammation. In prostate cancer, Boswellia inhibits prostate tumor growth.
Boswellic acid shown to have systemic anti-inflammatory effects through topical application. This study only looked at Boswellia Serrata and it's triterpenes. The different Boswellia have different levels of AKBA, BA, and BKA.
marine n-3 PUFAs have also been shown to alter the production of inflammatory proteins including chemokines, cytokines, growth factors and matrix proteases
Two transcription factors that are likely to play a role in inflammation are nuclear factor κ B (NFκB) and PPAR-γ
NFκB is the principal transcription factor involved in upregulation of inflammatory cytokine, adhesion molecule and cyclooxygenase-2 genes
PPAR-γ, is believed to act in an anti-inflammatory manner
PPAR-γ directly regulates inflammatory gene expression, it also interferes with the activation of NFκB creating an intriguing interaction between these two transcription factors
Both NFκB and PPAR-γ may be regulated by n-3 PUFAs.
great review of the anti-inflammatory effects of omega 3 DHA and EPA. EPA inhibits COX and 5-LOX and their downstream prostaglandin and leukotrienes. EPA/DHA inhibited endotoxin-stimulated IL-6, IL-8,TNF-alpha, and NFkappaB.
The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
DHA deficiency further elevates TBI-induced production of SBDPs
less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
In this study, the benefits of Testosterone was found to reduce 5-LO activity. This has implications in CVD in men. No evidence was found for 5alpha-DHT.