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Igent, tudok róla.
Experminetális körülmények között jó eredményt észleltek, emberben az alkalmazásának még több akadálya van (mellékelem egy részét az ismereteknek).
Egyébként a szelénről bizonyított ez a hatás és alkalmazható, be is szerezhető.
The Effect of Selenium Therapy
on Autoimmune Thyroiditis

CSABA BALÁZS, JÁNOS FEHÉR
Abbreviations
AT = autoimmune thyroiditis; n. s. = not significant; Se = selenium; T2 = di-iodothyronine; T3 = tri-iodothy-
ronine; T4 = thyroxine; fT3 = free tri-iodothyronine; fT4 = free thyroxine; TAS = total antioxidant status; TG
= thyroglobulin; TSH = thyroid-stimulating hormone; TPO = thyroid peroxidase enzyme; vs. = versus269
n
DOI:10.1556/CEMED.3.2009.284082009

Department of Medicine & Endocrinology,
Polyclinic of the Hospitaller Brother’s of St. John of God in Buda, Budapest Department of Internal Medicine,Semmelweis University Medical School, Budapest, Hungary
Due to its antioxidant capacity, the essential trace element selenium exerts complex effects on
the endocrine and immune systems. Selenium may have an important role in autoimmune
thyroid diseases because levels of free oxygen radicals are elevated during physiological thyroid
hormone synthesis. Objective: To determine whether selenium therapy can influence anti-thyroid
peroxidase and anti-thyroglobulin antibody levels or if there is a correlation between
antioxidant capacity and autoantibody titres. Method: 132 patients with autoimmune thyroiditis
were investigated in a prospective, blinded and placebo controlled study. L-thyroxine substitution
therapy was administered in both groups and TSH levels remained in the normal
range. The selenium treated group (70 patients, 68 female, mean age 41.4 ! 9.5 years) was
compared with the placebo treated group (62 patients, 61 female, mean age 42.7 ! 8.3
years). Selenium therapy included oral administration of 100 µg L-seleno-methionine tablets
twice a day for a year. Determinations of TSH, fT4 and fT3 as well as antibody levels were carried
out by chemoluminescent method. Total antioxidant capacity was determined by Randox
kit, and serum selenium levels were measured by atomic absorption technique. In the course
of the study patients were controlled every third month and at the end of the one year long
observation period. Results: Selenium levels in untreated patients were significantly lower than
those in treated patients and controls. The fT3/fT4 ratio proved to be higher in patients after
selenium therapy. Titres of antithyroid antibodies (mostly antithyroid peroxidase) significantly
decreased at the end of the study. An inverse correlation was found between antioxidant
capacity and antithyroid peroxidase levels. The volume of thyroid gland slightly diminished in
treated patients. No adverse reactions were observed. Conclusion: Selenium completed with
L-thyroxine is a suitable therapy of patients with autoimmune thyroiditis.
Keywords: selenium, autoimmune thyroiditis, antithyroid peroxidase enzyme antibodies,
total antioxidant capac

Anatabine Ameliorates Experimental Autoimmune Thyroiditis
Patrizio Caturegli,
Alessandra De Remigis,
Marcella Ferlito,
Melissa A. Landek-Salgado,
Shintaro Iwama,
Shey-Cherng Tzou and
Paul W. Ladenson
-
Author Affiliations
Department of Pathology (P.C., A.D.R., M.A.L.-S., S.I., S.-C.T.), and Divisions of Endocrinology and Metabolism (P.C., P.W.L.) and Cardiology (M.F.), Department of Medicine, Johns Hopkins University School of Medicine, and Feinstone Department of Molecular Microbiology and Immunology (P.C.), Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland 21205
Address all correspondence and requests for reprints to: Patrizio Caturegli, M.D., M.P.H., Department of Pathology, Johns Hopkins University School of Medicine, Ross 656, 720 Rutland Avenue, Baltimore, Maryland 21205. E-mail: pcat@jhmi.edu.
Abstract

Tobacco smoking favorably influences the course of Hashimoto thyroiditis, possibly through the antiinflammatory proprieties of nicotine. In this study we tested anatabine, another tobacco alkaloid, in a model of experimental autoimmune thyroiditis. Experimental autoimmune thyroiditis was induced by different doses of thyroglobulin, to produce a disease of low, moderate, or high severity, in 88 CBA/J female mice: 43 drank anatabine supplemented water and 45 regular water. Mice were bled after immunization and killed to assess thyroid histopathology, thyroglobulin antibodies, T4, and thyroid RNA expression of 84 inflammatory genes. We also stimulated in vitro a macrophage cell line with interferon-γ or lipopolysaccharide plus or minus anatabine to quantitate inducible nitric oxide synthase and cyclooxygenase 2 protein expression. Anatabine reduced the incidence and severity of thyroiditis in the moderate disease category: only 13 of 21 mice (62%) developed thyroid infiltrates when drinking anatabine as compared with 22 of 23 (96%) controls (relative risk 0.59, P = 0.0174). The median thyroiditis severity was 0.5 and 2.0 in anatabine and controls, respectively (P = 0.0007 by Wilcoxon rank sum test). Anatabine also reduced the antibody response to thyroglobulin on d 14 (P = 0.029) and d 21 (P = 0.045) after immunization and improved the recovery of thyroid function on d 21 (P = 0.049). In the thyroid transcriptome, anatabine restored expression of IL-18 and IL-1 receptor type 2 to preimmunization levels. Finally, anatabine suppressed in a dose-dependent manner macrophage production of inducible nitric oxide synthase and cyclooxygenase 2. Anatabine ameliorates disease in a model of autoimmune thyroiditis, making the delineation of its mechanisms of action and potential clinical utility worthwhile.

Tobacco smoking has numerous detrimental effects on human health, but it has also been associated with a few apparent salutary actions, including the amelioration of autoimmune (Hashimoto) thyroiditis and ulcerative colitis. Smokers in the Third National Health and Nutrition Examination Survey were found to have lower prevalence of thyroperoxidase and/or thyroglobulin antibodies than nonsmokers (1). This protective effect of smoking was confirmed in two additional cross-sectional studies, one from the Amsterdam autoimmune thyroid disease cohort (2) and the other from the Danish population (3), as well as in a 5-yr prospective study also based on the Amsterdam autoimmune thyroid disease cohort (4). In the prospective study, cigarette smoking women who had one or more relative with documented thyroid autoimmunity but no thyroid dysfunction or autoantibodies at study entry showed lower odds of developing thyroperoxidase and/or thyroglobulin antibodies (4). Similarly in ulcerative colitis, smoking has been shown to decrease flares (5), hospitalizations (6), and a need for oral glucocorticoids (7) so that low-dose smoking resumption has been successfully used in ex-smokers with refractory disease (8).

The mechanisms underlying this influence of tobacco smoking on some autoimmune diseases have been related to the effects of tobacco components on the immune system (9). There are numerous (>4000) components in tobacco, including alkaloids (such as nicotine and anatabine), gases (e.g. carbon monoxide), and carcinogens (e.g. polycyclic aromatic hydrocarbons, aldehydes, free radicals, and solvents), and of them nicotine is known to possess antiinflammatory properties (10). Nicotine acts via binding to the nicotinic receptor, a pentameric ion channel (mainly for sodium and calcium) formed by the arrangement of 16 different subunits in hetero- or homomeric conformations (11). The receptor is classically expressed in the peripheral (all preganglionic fibers and neuromuscular synapses) and central nervous system, but more recently it has been described in cells of the immune system, including CD4 T lymphocytes, dendritic cells, and macrophages (12). Indeed, the α7-homopentameric nicotinic receptor has emerged as a novel therapeutic target for diseases with an inflammatory pathogenesis (13).

Nicotine has been used successfully in mice with experimental autoimmune encephalomyelitis in which it reduced disease severity, shifting the autoimmune profile from pathogenic Th1 and Th17 responses to protective Th2 responses (14). Nicotine, however, cannot be used in humans because it is addictive and toxic and has a short 3-h plasma half-life. Consequently, we reasoned that other alkaloids of tobacco could share similar antiinflammatory properties but have a more favorable pharmacological profile. The minor tobacco alkaloid anatabine is nonaddictive and nontoxic at therapeutic doses and has a longer 8-hr half-life. Furthermore, anatabine has been recently shown to inhibit nuclear factor-κB (NF-κB) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15). In the present study, we therefore tested the antiinflammatory properties of anatabi

Hasonló módon az alábbi készítmény is a jövő "zenéje" lehet.
Az astaxanthin és a szív
A C-reaktív proteint (CRP) a tudósok a szívbetegségek koleszterinnél megbízhatóbb
indikátoraként kezelik. Ha a testben gyulladásos folyamatok játszódnak le, a máj és a
koszorúserek CRP-t termelnek és azt a vérbe juttatják. 2006-ban egy klinikai
tanulmányban megvizsgálták a természetes astaxanthin vér CRP- szintjére gyakorolt
hatását. A vizsgálatot egy természetes anyagok klinikai tanulmányaira szakosodott
független kutató vállalat, a kaliforniai Health Research and Studies Center végezte. A
tanulmányt PhD Gene Spiller vezette. Dr. Spiller már korábban is végzett a
természetes astaxanthinnal kapcsolatos vizsgálatokat. Ebben a vizsgálatban nyolc
héten keresztül 25 vizsgálati alany vett részt. Közülük tizenhatan természetes
astaxanthint, kilencen pedig placebót kaptak. A vér CRP- szintjét a tanulmány
kezdetén és végén állapították meg. Az eredmények igen pozitívak voltak: Az
astaxanthin - csoportnál a CRP 20,7%-os csökkenését mérték. A placebo -csoportnál
ezzel szemben a CRP-értékek növekedése volt megfigyelhet
ı. A kutatók az alábbi
következtetést vonták le: Az astaxanthin csökkentheti a szívbetegségek kockázatát.

Jó egészséget kívánok:


Prof. Dr. Balázs Csaba
2013-11-26 13:30:56