Olive Oil Phenolic Compounds Decrease The Rise In Plasma Endotoxin Levels After Breakfast

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Food Chem. 2014 Nov 1;162:161-71. doi: 10.1016/j.foodchem.2014.04.047. Epub 2014 Apr 24.

Olive oil phenolic compounds decrease the postprandial inflammatory response by reducing postprandial plasma lipopolysaccharide levels.

Camargo A1, Rangel-Zuñiga OA2, Haro C2, Meza-Miranda ER2, Peña-Orihuela P2, Meneses ME2, Marin C2, Yubero-Serrano EM2, Perez-Martinez P2, Delgado-Lista J2, Fernandez-Real JM3, Luque de Castro MD4, Tinahones FJ5, Lopez-Miranda J2, Perez-Jimenez F2.

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Abstract

We investigated the molecular mechanisms by which phenolic compounds (phenols) in virgin olive oil reduce the postprandial inflammatory response with the aim of identifying the transcription factor involved and the downstream effects. Olive oil-based breakfasts prepared with virgin olive oil (VOO) with high (398 ppm), intermediate (149 ppm) and low (70 ppm) phenol content were administered to 49 metabolic syndrome patients following a randomized crossover design. The consumption of a high-phenol VOO-based breakfast limited the increase of lipopolysaccharide plasma levels, TLR4, and SOCS3 proteins (p<0.001, p=0.041 and p=0.008, respectively), the activation of NF-κB (p=0.016) and the IL6 (p=0.007 and p=0.048, low and intermediate oil, respectively), IL1B (p=0.002, intermediate oil), and CXCL1 (p=0.001) postprandial gene expression, in peripheral blood mononuclear cells, as compared with the consumption of a breakfast prepared with the same oil but with low or intermediate phenol content. Virgin olive oil phenolic compounds reduce the postprandial inflammatory response in association with postprandial plasma lipopolysaccharide levels.

KEYWORDS:

Inflammation; Lipopolysaccharides; Phenolic compounds; Toll-like receptor; Transcription factor; Virgin olive oil

Olive oil phenolic compounds decrease the postprandial inflammatory response by reducing postprandial plasma lipopolysaccharide levels. - PubMed - NCBI
 
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Makes me think of 105 year old Japanese Dr. Hinohara...I like his diet...notice his breakfast....

"For breakfast I drink coffee, a glass of milk and some orange juice with a tablespoon of olive oil in it. Olive oil is great for the arteries and keeps my skin healthy. Lunch is milk and a few cookies, or nothing when I am too busy to eat. I never get hungry because I focus on my work. Dinner is veggies, a bit of fish and rice, and, twice a week, 100 grams of lean meat."
 
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Logan-

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Also ginger:

Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 914563, 9 pages
http://dx.doi.org/10.1155/2013/914563

Research Article
Dried Ginger (Zingiber officinalis) Inhibits Inflammation in a Lipopolysaccharide-Induced Mouse Model

Abstract

Objectives. Ginger rhizomes have a long history of human use, especially with regards to their anti-inflammatory properties. However, the mechanisms by which ginger acts on lipopolysaccharide-(LPS-)induced inflammation have not yet been identified. We investigated the anti-inflammatory effects of dried Zingiber officinalis (DZO) on LPS-induced hepatic injury. Methods. ICR mice were given a DZO water extract (100, 1000 mg/kg) orally for three consecutive days. On the third day, they were administered by LPS intraperitoneally. To investigate the anti-inflammatory effects of DZO, histological, cytokine expression, and protein factor analyses were performed. Results. Oral administration of DZO significantly reduced pathological changes in the liver and proinflammatory cytokines including interferon-(IFN-)γ and interleukin-(IL-)6 in the serum. In addition, DZO inhibited LPS-induced NF-κB activation by preventing degradation of the IκB-α, as well as the phosphorylation of ERK1/2, SAPK/JNK, and p38 MAPKs. These were associated with a decrease in the expression of inducible nitric oxide synthase (iNOS) and cyclooxyenase-2 (COX-2). Conclusions. Our data provide evidence for the hepatoprotective mechanisms of DZO as an anti-inflammatory effect. Furthermore, use of DZO to treat could provide therapeutic benefits in clinical settings.

...

Discussion

We demonstrated that pretreatment with DZO significantly reduced the inflammatory response of LPS-induced inflammation. LPS induced liver-related inflammation in a mouse model of viral hepatitis that closely resembles human viral hepatitis [18]. A previous study reported that LPS-induced histological changes showed lymphocyte and neutrophil infiltration increasing in the central and portal areas [19]. Our histological analysis showed the inhibitory effects of DZO on necrotic hepatocytes and tissue damage with excessive production of inflammatory cytokines in the LPS-induced liver and serum. In particular, DZO1000 group largely attenuated LPS-induced broad hemorrhagic necrosis of liver structure similar to normal group. These results indicate that DZO is effective for controlling the response of LPS-induced liver damage.

Several studies have indicated that the inflammatory response to LPS challenge is associated with the release of pro-inflammatory cytokines such as IFN-γ and IL-6 [20]. In addition, mediators generated by LPS stimulation assist the innate immune response, but their overproduction results in acute inflammation that can cause tissue injury and organ failure [21]. Here, we confirmed that DZO inhibits the expression of LPS-induced IFN-γ and IL-6, which are significantly elevated in LPS-induced inflammation. These results indicate that DZO might suppress the inflammatory response via the inhibition of inflammatory cytokines supporting our histological analysis.

The transcription regulator NF-κB plays a pivotal role in activating subsequent signaling pathways, especially the regulation of pro-inflammatory molecules [22]. Also, activation of LPS-induced NF-κB causes phosphorylation of IκB-α kinase (IKK), leading to degradation of IκB-α and translocation of NF-κB into the nucleus [23]. These studies may provide a target to specifically downregulate the expression of NF-κB with inhibition of IκB-α degradation. In this study, DZO inhibited LPS-induced NF-κB transcription activity as well as IκB-α protein expression in the liver compared to negative control group.

Many studies have reported that MAPKs mediate the activation of the transcription factor NF-κB [24]. To explore the mechanisms of NF-κB inactivation by DZO, the effects of DZO on LPS-induced phosphorylation of the Erk1/2, SAPK/JNK, and p38 MAP kinases were examined. All of the kinases were overexpressed after exposure to LPS, but that expression was reduced after DZO exposure. This suggests that the hepatoprotective activity of DZO is due to NF-κB inhibition via the inhibition of LPS-induced phosphorylation of MAPKs.

Furthermore, NF-κB activation mediates the expression of rapid-response genes, including pro-inflammatory mediators such as iNOS and COX-2 [25]. The present study confirmed that LPS stimulates iNOS and COX-2, which was associated with overexpression of NF-κB, whereas orally administrated DZO greatly reduces the expression of iNOS and COX-2 and hence the expression of NF-κB. It is likely that the anti-inflammatory activity of DZO contributes to the reduced expression of iNOS and COX-2 in LPS-induced liver injury. Also, proinflammation cytokines, IL-6 and TNF-α are upregulated by the expression of COX-2 and iNOS [26]. Taken together, these data suggest that DZO inhibits the expression of iNOS and COX-2 through inactivation of NF-κB by reducing IκB-α phosphorylation. We assume that the hepatoprotective effects of DZO may be due to the anti-inflammatory compounds such as gingerols and shogaols. These results are helpful in understanding the anti-inflammations properties of DZO.

Conclusion

We found that DZO inhibits LPS-induced inflammation via regulation of NF-κB and MAP kinases. DZO significantly inhibits the production of IFN-γ and IL-6 and suppresses NF-κB by degradation of IκB-α. These activities appear to be mediated via downregulation of the ERK1/2, SAPK/JNK, and p38 MAP kinases signaling pathways and suppression of iNOS and COX-2. Our data provide evidence for a mechanism by which DZO acts as an anti-inflammatory agent. Strategic use of DZO in treating inflammatory diseases could provide therapeutic benefits for future clinical use.
 
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LeeLemonoil

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The same benefits of the phenolic compounds provides olive leaf tea, if your diet is too high in fat.

Hydroxytyrosol, Tyrosol, Oleuropein, Oleocanthal.
All 4 are pro-metabolic, androgenic, anti-estrogenic, anti-imflammatory.
 
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Effects of Methylene Blue on endotoxin administration:

Acta Anaesthesiol Scand. 2001 Nov;45(10):1246-54.
Continuously infused methylene blue modulates the early cardiopulmonary response to endotoxin in awake sheep.
Evgenov OV1, Sveinbjørnsson B, Bjertnaes LJ.
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Abstract

BACKGROUND:
In endotoxemia and septic shock, enhanced generation of endogenous nitric oxide (NO) contributes to myocardial depression, hypotension, and derangement of gas exchange. We hypothesized that continuous infusion of methylene blue (MB), an inhibitor of the NO pathway, would counteract these effects in endotoxemic sheep.

METHODS:
Twenty-one sheep were anesthetized and instrumented for a chronic study with vascular catheters. On the day of the experiment, 18 conscious animals randomly received either an intravenous injection of MB 10 mg x kg(-1) or isotonic saline. Thirty minutes later, sheep received a 20-min intravenous infusion of Escherichia coli endotoxin 1 microg x kg(-1) and either an intravenous infusion of MB 2.5 mg x kg(-1) x h(-1) or isotonic saline, respectively, for 5 h. In addition, 3 animals were exposed to the same dose of MB alone.

RESULTS:
MB reduced the early endotoxin-induced declines in stroke volume, left ventricular stroke work and cardiac indices, and prevented mean arterial pressure from falling. Moreover, MB ameliorated the increases in pulmonary arterial pressure and pulmonary vascular resistance index. In addition, MB reduced the increments in venous admixture and AaPO2, decreased the falls in PaO2, SaO2, and oxygen delivery, and maintained oxygen consumption. MB also prevented the rises in body temperature and plasma nitrites and nitrates, and delayed the elevation of plasma lactate. When given alone to healthy sheep, MB transiently reduced plasma lactate and PaO2, and increased AaPO2.

CONCLUSION:
In ovine endotoxemia, continuously infused MB counteracts the early myocardial dysfunction and derangement of hemodynamics and gas exchange.

Continuously infused methylene blue modulates the early cardiopulmonary response to endotoxin in awake sheep. - PubMed - NCBI
 

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