Prävention und Therapie bei Entzündungen

Abb. 1 Rote Weintrauben enthalten Resveratrol, das u. a. antientzündliche Wirkung aufweist. Quelle: Rike/PIXELIO.

Entzündliche Mechanismen sind nach heutiger Kenntnis an allen bedeutenden chronischen Krankheiten beteiligt, wenn nicht deren Ursache. Dies trifft nicht nur für die klassischen chronischen Entzündungskrankheiten wie rheumatoide Arthritis, Kollagenosen, Morbus Crohn oder multiple Sklerose zu, sondern ebenso für die atypischen inflammatorischen Erkrankungen wie Adipositas, metabolisches Syndrom, Arteriosklerose, Hypertonus, Herzinfarkt, Schlaganfall, Krebserkrankungen, Neurodegeneration, Alzheimer [10], endogene Depression und selbst für den Alterungsprozess, für den der Begriff „Inflammaging“ geprägt wurde [12].

Nach erfolgreicher Elimination einer Noxe muss im typischen Erkrankungsfall das Entzündungsprogramm möglichst effektiv beendet werden, um Schäden für den betroffenen Organismus zu vermeiden. Das hierfür verfügbare antientzündliche Repertoire ist ähnlich umfangreich wie die proentzündlichen Mechanismen und wirkt selbstlimitierend. Bei den chronischen Entzündungskrankheiten gilt es in erster Linie, die inflammatorische Aktivität zu limitieren bzw. bei den atypischen Erkrankungen, den Entzündungstrigger zu identifizieren und durch primär oder sekundär präventive Maßnahmen möglichst frühzeitig zu eliminieren, um unausweichliche spätere Schäden zu vermeiden.

Literatur

• 1 Anand P, Sundaram C, Jhurani S. et al . Curcumin and cancer: an “old-age” disease with an “age-old” solution.  Cancer Lett. 2008;  267 133-164
• 2 Babu P V, Liu D. Green tea catechins and cardiovascular health: an update.  Curr Med Chem. 2008;  15 1840-1850
• 3 Boots A W, Wilms L C, Sweenen E L, Kleinjans J C, Bast A, Haenen G R. In vitro and ex vivo anti-inflammatory activity of quercetin in healthy volunteers.  Nutrition. 2008;  24 703-710
• 4 Bosscher de K, Berghe van den W, Haegeman G. The interplay between the glucocorticoid receptor and nuclear factor-kappaB or activator protein-1: molecular mechanisms for gene repression.  Endocr Rev. 2003;  24 488-522
• 5 Boswellia serrata. Monograph.  Altern Med Rev. 2008;  13 165-167
• 6 Breslow J L. n-3 Fatty acids and cardiovascular disease.  Am J Clin Nutr. 2006;  83 (Suppl) 1477S-1482S
• 7 Calabro P, Yeh E T. Obesity, inflammation, and vascular disease: the role of the adipose tissue as an endocrine organ.  Subcell Biochem. 2007;  42 63-91
• 8 Calder P. n-3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases.  Am J Clin Nutr. 2006;  83 (Suppl) 1505S-1519S
• 9 Charo I F, Ransohoff R M. The many roles of chemokines and chemokine receptors in inflammation.  New Engl J Med. 2006;  354 610-621
• 10 Casserly I, Topol E. Convergence of atherosclerosis and Alzheimer's disease: inflammation, cholesterol, and misfolded proteins.  Lancet. 2004;  363 1139-1146
• 11 Devaraj S, Leonard S, Traber M G, Jialal I. Gamma-tocopherol supplementation alone and in combination with alpha-tocopherol alters biomarkers of oxidative stress and inflammation in subjects with metabolic syndrome.  Free Radic Biol Med. 2008;  44 1203-1208
• 12 Franceschi C. Inflammaging as a major characteristic of old people: can it be prevented or cured?.  Nutr Rev. 2007;  65 S173-S176
• 13 Giannoulis-Karantara A, Vlachou A, Polychronopoulou S, Papassotiriou I, Chrousos G Pl. Melatonin and immunomodulation: connections and potential clinical applications.  Neuroimmunomodulation. 2006;  13 133-144
• 14 Goodfellow J, Bellamy M F, Ramsey M W, Jones C J, Lewis M J. Dietary supplementation with marine omega-3 fatty acids improve systemic large artery endothelial function in subjects with hypercholesterolemia.  J Am Coll Cardiol. 2000;  35 265-270
• 15 Hämälainen M, Nieminen R, Vuorela P, Heinonen M, Moilanen E. Anti-inflammatory effects of flavonoids: genistein, kaempferol, quercetin, and daidzein inhibit STAT-1 and NF-kappaB activations, whereas flavone, isorhamnetin, naringenin, and pelargonidin inhibit only NF-kB activation along with their inhibitory effect on iNOS expression and NO production in activated macrophages.  Mediators Inflamm. 2007;  ID 45673 1-10
• 16 Hankey G J, Eikelboom J W. Aspirin resistance.  Lancet. 2006;  367 606-617
• 17 Hansson G K. Inflammation, atherosclerosis, and coronary artery disease.  New Engl J Med. 2005;  352 1685-1695
• 18 Harris S G, Padilla J, Koumas L, Ray D, Phipps R P. Prostaglandins as modulators of immunity.  Tr Immunol. 2002;  23 144-150
• 19 Hatcher H, Planalp R, Cho J. et al . Curcumin: from ancient medicine to current clinical trials.  Cell Mol Life Sci. 2008;  65 1631-1652
• 20 Jurenka J S. Therapeutic applications of pomegranate (Punica granatum): a review.  Altern Med Rev. 2008;  13 128-144
• 21 Kaisho T, Tanaka T. Turning NF-kB and IRFs on and off in DC.  Tr Immunol. 2008;  29 329-336
• 22 Karlsec A, Rettersol L, Laake P. et al . Anthocyanins inhibit nuclear factor-kB activation in monocytes and reduce olasma concentrations of pro-inflammatory mediators in healthy adults.  J Nutr. 2007;  137 1951-1954
• 23 Lambert C P, Wright N R, Finck B N, Villareal D T. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese eldely persons.  J Appl Physiol. 2008;  105 473-478
• 24 Lansky E P, Newman R A. Punica franatum (pomegranate) and its potential for prevention and treatment of infammation and cancer.  J Ethnopharmacol. 2007;  109 177-206
• 25 Mihm S, Galter D, Dröge W. Modulation of transcription factor NF-kB activity by intracellular glutathione levels and by variations of the extracellular cysteine supply.  Faseb J. 1995;  9 246-252
• 26 Müller N, Schwarz M J. A psychoneuroimmunological perspective to Emil Kraepelins dichotomy. Schizophrenia and major depression as inflammatory CNS disorders.  Eur Arch Psychiatry Neurosci. 2008;  258 (Suppl 2) 97-106
• 27 Murakami A, Ashida H, Terao J. Multitargeted cancer prevention by quercetin.  Cancer Lett. 2008;  269 315-325
• 28 Murias M, Handler N, Erker T. et al . Resveratrol analogues as selective cyclooxygenase-2 inhibitors: snythesis and structure-activity relationship.  Bioorg Med Chem. 2004;  12 5571-5578
• 29 Pascual G, Glass C K. Nuclear receptors versus inflammation: mechanisms of transrepression.  Trends Endocrinol Metab. 2006;  17 321-327
• 30 Petersen A MW, Pedersen B K. The role of IL-6 in mediating the antiinflammatory effects of exercise.  J Physiol Pharmacol. 2006;  57 (Suppl 10) 43-51
• 31 Rainsford K D. Anti-inflammatory drugs in the 21st century.  Subcell Biochem. 2007;  42 3-27
• 32 Redwine L, Hauger R L, Gillin J C, Irwin M. Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans.  J Clin Endocrinol Metab. 2000;  85 3597-3603
• 33 Sears B. The antiinflammation zone: reversing the silent epidemic that's destroying our health. Regan Books 2005
• 34 Serhan C N, Brain S D, Buckley C D. et al . Resolution of inflammation: state of the art, definitions and terms.  Faseb J. 2007;  21 325-332
• 35 Shoelson S E, Lee J, Goldfine A B. Inflammation and insulin resistance.  J Clin Invest. 2006;  116 1793-1801
• 36 Song Y, Li T Y, van Dam R M, Manson J E, Hu F B. Magnesium intake and plasma concentrations of markers of systemic inflammation and endothelial dysfunction in women.  Am J Clin Nutr. 2007;  85 1068-1074
• 37 Takada Y, Bhardwaj A, Potdar P, Aggarwal B B. Nonsteroidal anti-inflammatory agents differ in their ability to suppress NF-kB activation, inhibition of cyclooxygenase-2 and cyclin-1, and abrogation of tumor cell proliferation.  Oncogene. 2004;  23 9247-9258
• 38 Tracey K J. Physiology and immunology of the cholinergic antiinflammatory pathway.  J Clin Invest. 2007;  117 289-296
• 39 Vegeto E, Benedusi V, Maggi A. Estrogen anti-inflammatory activity in brain: a therapeutic opportunity for menopause and neurodegenerative diseases.  Front Neuroendocrinol. 2008;  29 507-519
• 40 Zhang W J, Frei B. Alpha-lipoic acid inhibits TNF-alpha induced NF-kB activation and adhesion molecule-1 expression in huma aortic endothelial cells.  Faseb J. 2001;  15 2423-2432