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| Science Forum Index » Life Extension Forum » Chemical wars against arachidonic acid: Mice making... |
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| Taka... |
 Posted: Fri Jul 03, 2009 7:01 am |
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Guest
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Transgenic mice rich in endogenous omega-3 fatty acids are protected
from colitis
Omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFA) are
the precursors of potent lipid mediators and play an important role in
regulation of inflammation. Generally, n-6 PUFA promote inflammation
whereas n-3 PUFA have antiinflammatory properties, traditionally
attributed to their ability to inhibit the formation of n-6 PUFA-
derived proinflammatory eicosanoids. Newly discovered resolvins and
protectins are potent antiinflammatory lipid mediators derived
directly from n-3 PUFA with distinct pathways of action. However, the
role of the n-3 PUFA tissue status in the formation of these
antiinflammatory mediators has not been addressed. Here we show that
an increased n-3 PUFA tissue status in transgenic mice that
endogenously biosynthesize n-3 PUFA from n-6 PUFA leads to significant
formation of antiinflammatory resolvins and effective reduction in
inflammation and tissue injury in colitis. The endogenous increase in
n-3 PUFA and related products did not decrease n-6 PUFA-derived lipid
mediators such as leukotriene B4 and prostaglandin E2. The observed
inflammation protection might result from decreased NF-êB activity and
expression of TNFá, inducible NO synthase, and IL-1â, with enhanced
mucoprotection probably because of the higher expression of trefoil
factor 3, Toll-interacting protein, and zonula occludens-1. These
results thus establish the fat-1 transgenic mouse as a new
experimental model for the study of n-3 PUFA-derived lipid mediators.
They add insight into the molecular mechanisms of inflammation
protection afforded by n-3 PUFA through formation of resolvins and
protectins other than inhibition of n-6 PUFA-derived eicosanoid
formation.
SOURCE: http://www.pnas.org/content/103/30/11276.full
doi: 10.1073/pnas.0601280103 |
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| John Hasenkam... |
| Posted: Sat Jul 04, 2009 12:23 am |
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There you go Taka, just this week I read two articles indicating that this
genetic strain also has increased susceptibility to retinal degeneration and
that 4HHE, the oxidation of DHA, being one of the culprits. I accept those
results because I found other supporting evidence but as a general rule I'm
rather wary of transgene studies.
John.
"Taka" <taka0038 at (no spam) gmail.com> wrote in message
news:dd60a0db-cb9f-410b-9f8e-acf1d5696841 at (no spam) p29g2000yqh.googlegroups.com...
Transgenic mice rich in endogenous omega-3 fatty acids are protected
from colitis
Omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFA) are
the precursors of potent lipid mediators and play an important role in
regulation of inflammation. Generally, n-6 PUFA promote inflammation
whereas n-3 PUFA have antiinflammatory properties, traditionally
attributed to their ability to inhibit the formation of n-6 PUFA-
derived proinflammatory eicosanoids. Newly discovered resolvins and
protectins are potent antiinflammatory lipid mediators derived
directly from n-3 PUFA with distinct pathways of action. However, the
role of the n-3 PUFA tissue status in the formation of these
antiinflammatory mediators has not been addressed. Here we show that
an increased n-3 PUFA tissue status in transgenic mice that
endogenously biosynthesize n-3 PUFA from n-6 PUFA leads to significant
formation of antiinflammatory resolvins and effective reduction in
inflammation and tissue injury in colitis. The endogenous increase in
n-3 PUFA and related products did not decrease n-6 PUFA-derived lipid
mediators such as leukotriene B4 and prostaglandin E2. The observed
inflammation protection might result from decreased NF-êB activity and
expression of TNFá, inducible NO synthase, and IL-1â, with enhanced
mucoprotection probably because of the higher expression of trefoil
factor 3, Toll-interacting protein, and zonula occludens-1. These
results thus establish the fat-1 transgenic mouse as a new
experimental model for the study of n-3 PUFA-derived lipid mediators.
They add insight into the molecular mechanisms of inflammation
protection afforded by n-3 PUFA through formation of resolvins and
protectins other than inhibition of n-6 PUFA-derived eicosanoid
formation.
SOURCE: http://www.pnas.org/content/103/30/11276.full
doi: 10.1073/pnas.0601280103 |
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