Proteins in Bone Health, Development and Disease in Environmental Illness

Proteins in Bone Health, Development and Disease in Environmental Illness

Wine Compound Improves Symptom of CFS - Study

Wine Compound Improves Symptom of CFS - Study

Assessment of 3-nitropropionic acid-evoked peripheral neuropathy in rats: neuroprotective effects of acetyl-l-carnitine and resveratrol.

"resveratrol is a good candidate for treatment of metabolic neuropathy. The experimental outcome of this study shows that chronic treatment with 3-NPA in rats is relevant in development of an experimental model of toxic neuropathy."

Read more: CiteULike: Assessment of 3-nitropropionic acid-evoked peripheral neuropathy in rats: neuroprotective effects of acetyl-l-carnitine and resveratrol.:

Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase

Comment: I may forgetting something -- but this might be a possible benefit of polyphenols from red wine in combatting some of the effects of cigarette smoke and combustable pollutants?


Red wine polyphenols prevent endothelial dysfunction induced by endothelin-1 in rat aorta: role of NADPH oxidase

Resveratrol differentially modulates inflam responses of microglia & astrocytes

Comment: An extremely useful read for those interested in this kind of stuff. Full text available.

"the first report of a difference between microglial cell and astrocyte in response to LPS, and of a difference in the capacity of resveratrol to protect microglia and astrocytes from inflammatory insults."


Lu, X., Ma, L., Ruan, L., Kong, Y., Mou, H., Zhang, Z., Wang, Z., Wang, J. M., and Le, Y. (2010). Resveratrol differentially modulates inflammatory responses of microglia and astrocytes. Journal of Neuroinflammation, 7(1):46+.  http://www.citeulike.org/user/HEIRS/article/7694580

Nair, S., Barve, A., Khor, T.-O. O., Shen, G.-X. X., Lin, W., Chan, J. Y., Cai, L., and Kong, A.-N. N. (2010). Regulation of nrf2- and ap-1-mediated gene expression by epigallocatechin-3-gallate and sulforaphane in prostate of nrf2-knockout or c57bl/6j mice and pc-3 ap-1 human prostate cancer cells. Acta pharmacologica Sinica. http://www.citeulike.org/user/HEIRS/article/7694509

AKT/GSK-3beta/beta-catenin signalling within hippocampus and amygdala reflects genetically determined differences in posttraumatic stress disorder like symptoms.

"Taken together our study identifies lasting changes in the AKT/GSK-3beta/beta-catenin cascade within the hippocampus and amygdala as molecular correlates of genetically determined differences in the severity of PTSD-like symptoms."

CiteULike: AKT/GSK-3beta/beta-catenin signalling within hippocampus and amygdala reflects genetically determined differences in posttraumatic stress disorder like symptoms.:

Supplemental: Resveratrols, a compound found in wine and grapes exert their protective effects against neuronal damage and death are mediated throught this same pathway.

Fukui, M., Choi, H. J. J., and Zhu, B. T. T. (2010). Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death. Free radical biology & medicine, 49(5):800-813. http://www.citeulike.org/user/HEIRS/article/7301406
Xi, J., Wang, H., Mueller, R. A., Norfleet, E. A., and Xu, Z. (2009). Mechanism for resveratrol-induced cardioprotection against reperfusion injury involves glycogen synthase kinase 3beta and mitochondrial permeability transition pore. European journal of pharmacology, 604(1-3):111-116. http://www.citeulike.org/user/HEIRS/article/7588469

Tumor Necrosis Factor-Induced Neutrophil Adhesion Occurs Through SphK-1 Activation of Integrin

"TNFalpha activated endothelial cells being sphingosine kinase-1, alpha5beta1, and angiopoietin-2 dependent. Moreover, this work supports the notion that sphingosine kinase-1 may be the single target required for an effective broad spectrum approach to combat inflammation and immune disorders."

Tumor Necrosis Factor-Induced Neutrophil Adhesion ... [Am J Pathol. 2010] - PubMed result:

Researchers explain why red wine and green tea stop prostate cancer growth

"prostate cancer cell lines and mouse models to demonstrate that treatment with these dietary agents results in inhibition of the sphingosine kinase-1/sphingosine 1-phosphate (SphK1/S1P) pathway."
Researchers explain why red wine and green tea stop prostate cancer growth

Resveratrol Metabolites Induces HO-1 via Nrf2 through KEAP1 Residue Modification.

It is hence likely that piceatannol modifies specific cysteine residues of Keap1, which allows Nrf2 to translocate into the nucleus and bind to ARE, leading to enhancement of the expression of HO-1. The characteristic catechol moiety of piceatannol appears to be critical for induction of Nrf2 activation and subsequent upregulation of HO-1.

CiteULike: Piceatannol induces heme oxygenase-1 expression in human mammary epithelial cells through activation of ARE-driven Nrf2 signaling.: "Lee, H.-H. H., Park, S.-A. A., Almazari, I., Kim, E.-H. H., Na, H.-K. K., and Surh, Y.-J. J. (2010). Piceatannol induces heme oxygenase-1 expression in human mammary epithelial cells through activation of are-driven nrf2 signaling. Archives of biochemistry and biophysics."

CiteULike: Ameliorative potential of resveratrol on proinflammatory cytokines, hyperglycemia mediated oxidative stress, and pancreatic beta-cell dysfunction in streptozotocin-nicotinamide-induced diabetic rats.

CiteULike: Ameliorative potential of resveratrol on proinflammatory cytokines, hyperglycemia mediated oxidative stress, and pancreatic beta-cell dysfunction in streptozotocin-nicotinamide-induced diabetic rats.: "results of the present investigation demonstrated that resveratrol exhibits significant antidiabetic potential by attenuating hyperglycemia, enhancing insulin secretion and antioxidant competence in pancreatic beta-cells of diabetic rats"

Tregs, Il17 and the C5a receptor -- MOA in Chemical Sensitivity????

Background: Here is an addition to something I noted before...or at least postulated that resveratrol may have some interesting immune effects...and lately I have suggested that a loss of tolerance by alteration in T regulatory cells may have important implications in multiple chemical sensitivity.

The activation of cellular pathways can have both positive and negative inflammatory influence. As Ward describes, "C5a and is an extremely potent pro-inflammatory peptide that interacts with two C5a receptors, C5aR and C5L2, present on surfaces of phagocytes as well as other cell types. The former is a well-established receptor that initiates G-protein-coupled signaling via mitogen-activated protein kinase pathways. Its in vivo blockade greatly reduces inflammatory injury." We wrote last year that resveratrol has been demonstrated to have a somewhat mitigating effect on anaphylatoxin (C5) neutraphils in peritonitis that included a decrease in a number of immune indicators such as Tnf-a, Il-6, Il-1 etc. and are often upregulated in Nrf -/- mice. Generally, another study indicated how mast cells may amplify immune responses in allergic disease and that C5ar may be an important mechanism in mast cell pathologies. Most recently studies reveal the absense of C5a receptors in dendritic cells regulates the immune response through promotion of T regulatory cells and Th17.

Issuree, P. D. A., Pushparaj, P. N., Pervaiz, S., and Melendez, A. J. (2009). Resveratrol attenuates c5a-induced inflammatory responses in vitro and in vivo by inhibiting phospholipase d and sphingosine kinase activities. FASEB J., 23(8):2412-2424. http://www.citeulike.org/user/HEIRS/article/5338821
Soruri, A., Grigat, J., Kiafard, Z., and Zwirner, J. (2008). Mast cell activation is characterized by upregulation of a functional anaphylatoxin c5a receptor. BMC Immunology, 9:29+. http://www.citeulike.org/user/HEIRS/article/2904779
Weaver, D. J., Reis, E. S., Pandey, M. K., Köhl, G., Harris, N., Gerard, C., and Köhl, J. (2010). C5a receptor-deficient dendritic cells promote induction of treg and th17 cells. European Journal of Immunology, 9999(9999):NA+. http://www.citeulike.org/user/HEIRS/article/6614046
Thimmulappa, R. K., Lee, H., Rangasamy, T., Reddy, S. P., Yamamoto, M., Kensler, T. W., and Biswal, S. (2006). Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis. The Journal of clinical investigation, 116(4):984-995.
http://www.citeulike.org/user/HEIRS/article/3716756?show_msg=already_posted
Czermak, B. J., Sarma, V., Bless, N. M., Schmal, H., Friedl, H. P., and Ward, P. A. (1999). In vitro and in vivo dependency of chemokine generation on c5a and tnf-alpha. J Immunol, 162(4):2321-2325.
http://www.citeulike.org/user/HEIRS/article/6614341
Ward, P. A. (2009). Functions of c5a receptors. Journal of molecular medicine (Berlin, Germany), 87(4):375-378.
http://www.citeulike.org/user/HEIRS/article/4012763

Protective effect of resveratrol against LPS-induced extracellular lipoperoxidation in AR42J cells partly via a Myd88-dependent signaling pathway.

Protective effect of resveratrol against LPS-induced extracellular lipoperoxidation in AR42J cells partly via a Myd88-dependent signaling pathway.: "URL: Protective effect of resveratrol against LPS-induced extracellular lipoperoxidation in AR42J cells partly via a Myd88-dependent signaling pathway.

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Wine Component Reduces Inflammatory Pathway Mediation by Endotoxin

Summary: Resveratrol counteracted LPS effect by decreasing CD14 and IRAK1 expression but unexpectedly increased the p38 MAPK protein phosphorylation. Altogether, our data highlighted the functionality of the TLR4-Myd88 signaling pathway in LPS prooxidant effect using non myeloid cells.

Sebai, H., Ristorcelli, E., Sbarra, V., Hovsepian, S., Fayat, G., Aouani, E., and Lombardo, D. (2009). Protective effect of resveratrol against lps-induced extracellular lipoperoxidation in ar42j cells partly via a myd88-dependent signaling pathway. Archives of biochemistry and biophysics. http://www.citeulike.org/user/HEIRS/article/6457832

Arthritis: Synergistic Effect of Resveratrol and Curcumun on Inflammation

Title: Synergistic chondroprotective effects of curcumin and resveratrol in human articular chondrocytes: inhibition of interleukin-1beta-induced nuclear factor-kappab-mediated inflammation and apoptosis.

Summary: We propose that combining these natural compounds may be a useful strategy in OA therapy as compared to separate treatment with each individual compound.

Csaki, C., Mobasheri, A., and Shakibaei, M. (2009). Synergistic chondroprotective effects of curcumin and resveratrol in human articular chondrocytes: inhibition of interleukin-1beta-induced nuclear factor-kappab-mediated inflammation and apoptosis. Arthritis Research & Therapy, 11(6):R165+. http://www.citeulike.org/user/HEIRS/article/6067528

Central administration of resveratrol improves diet-induced diabetes.

Ramadori, G., Gautron, L., Fujikawa, T., Vianna, C. R., Elmquist, J. K., and Coppari, R. (2009). Central administration of resveratrol improves diet-induced diabetes. Endocrinology. http://www.citeulike.org/user/HEIRS/article/5947822

Brain Seems to Play Role in Resveratrol's Diabetes Effect

Brain Seems to Play Role in Resveratrol's Diabetes Effect

EGCG, Resveratrol and eNOS.

A new study has shown that EGCG attenuates the stimulation of heat shock protein 27 by GSK3b which results in lower bone resorption. In another post, we noted that GSK3b is stimulated by oxidative and that it can down-regulate Nrf2, sensitize cells to oxidants and results in the loss of tolerance to oxidants which occurs after long term exposure of oxidant exposure. This study notes that it is stimulated by sphingosine-1-phosphate. Another study has shown that one mechanism for resveratrol’s benefits is the attenuation of the C5 inflammatory response. This is achieved by resveratrol’s ability to inhibit sphingosine kinase activities and phospholipase D. Appeldoorn showed that in addition, resveratrol increases NO by 285%. In addition, he also showed that quercetin increased NO by 110%, epicatechingallate increased NO by 85% and epigallocatechingallate increased NO by 60%. It has been shown that cells that have higher eNOS have less chance of following the inflammatory cascade through NF-kappaB, are higher in PGC-1a and have lower reactive species generation from mitochondria.




Salazar, M., Rojo, A. I., Velasco, D., de Sagarra, R. M. M., and Cuadrado, A. (2006). Glycogen synthase kinase-3beta inhibits the xenobiotic and antioxidant cell response by direct phosphorylation and nuclear exclusion of the transcription factor nrf2. The Journal of biological chemistry, 281(21):14841-14851. http://www.citeulike.org/user/HEIRS/article/5360103



Rojo, A. I., Sagarra, M. R. d. R., and Cuadrado, A. (2008). Gsk-3beta down-regulates the transcription factor nrf2 after oxidant damage: relevance to exposure of neuronal cells to oxidative stress. Journal of neurochemistry, 105(1):192-202. http://www.citeulike.org/user/HEIRS/article/2608925



Appeldoorn, M. M., Venema, D. P., Peters, T. H. F., Koenen, M. E., Arts, I. C. W., Vincken, J.-P., Gruppen, H., Keijer, J., and Hollman, P. C. H. (0000). Some phenolic compounds increase the nitric oxide level in endothelial cells in vitro. Journal of Agricultural and Food Chemistry, 0(0). http://www.citeulike.org/user/HEIRS/article/5342745



Natsume, H., Adachi, S., Takai, S., Tokuda, H., Matsushima-Nishiwaki, R., Minamitani, C., Yamauchi, J., Kato, K., Mizutani, J., Kozawa, O., and Otsuka, T. (2009). (-)-epigallocatechin gallate attenuates the induction of hsp27 stimulated by sphingosine 1-phosphate via suppression of phosphatidylinositol 3-kinase/akt pathway in osteoblasts. International journal of molecular medicine, 24(2):197-203. http://www.citeulike.org/user/HEIRS/article/5343993



Issuree, P. D. A., Pushparaj, P. N., Pervaiz, S., and Melendez, A. J. (2009). Resveratrol attenuates c5a-induced inflammatory responses in vitro and in vivo by inhibiting phospholipase d and sphingosine kinase activities. FASEB J., 23(8):2412-2424. http://www.citeulike.org/user/HEIRS/article/5338821



Salazar, M., Rojo, A. I., Velasco, D., de Sagarra, R. M. M., and Cuadrado, A. (2006). Glycogen synthase kinase-3beta inhibits the xenobiotic and antioxidant cell response by direct phosphorylation and nuclear exclusion of the transcription factor nrf2. The Journal of biological chemistry, 281(21):14841-14851. http://www.citeulike.org/user/HEIRS/article/5360103