Спирулина Spirulina Научные исследования Спирулина в клинической практике: доказательства, основанные на человеческих приложений


Minimizing the cancer-promotional activity of cox-2 as a central strategy in cancer prevention



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  • Abstract

Minimizing the cancer-promotional activity of cox-2 as a central strategy in cancer prevention.


McCarty MF1.

  • 1NutriGuard Research, Inc., 1051 Hermes Ave., Encinitas, CA 92024, USA. markfmccarty@gmail.com

Abstract


A recent meta-analysis examining long-term mortality in subjects who participated in controlled studies evaluating the impact of daily aspirin on vascular risk, has concluded that aspirin confers substantial protection from cancer mortality. Remarkably, low-dose aspirin was as effective as higher-dose regimens; hence this protection may be achievable with minimal risk. There is reason to believe that this protection stems primarily from inhibition of cox-2 in pre-neoplastic lesions. Since safe aspirin regimens can only achieve a partial and transitory inhibition of cox-2, it may be feasible to complement the cancer-protective benefit of aspirin with other measures which decrease cox-2 expression or which limit the bioactivity of cox-2-derived PGE2. Oxidative stress boosts cox-2 expression by up-regulating activation of NF-kappaB and MAP kinases; NADPH oxidase activation may thus promote carcinogenesis by increasing cox-2 expression while also amplifying oxidant-mediated mutagenesis. A prospective cohort study has observed that relatively elevated serum bilirubin levels are associated with a marked reduction in subsequent cancer mortality; this may reflect bilirubin's physiological role as a potent inhibitor of NADPH oxidase. It may be feasible to mimic this protective effect by supplementing with spirulina, a rich source of a phycobilin which shares bilirubin's ability to inhibit NADPH oxidase. Ancillary antioxidant measures - phase 2 inducing phytochemicals, melatonin, N-acetylcysteine, and astaxanthin - may also aid cox-2 down-regulation. The cancer protection often associated with high-normal vitamin D status may be attributable, in part, to the ability of the activated vitamin D receptor to decrease cox-2 expression while promoting PGE2 catabolism and suppressing the expression of PGE2 receptors. Diets with a relatively low ratio of omega-6 to long-chain omega-3 fats may achieve cancer protection by antagonizing the production and bioactivity of PGE2. Growth factors such as IGF-I increase cox-2 expression by several complementary mechanisms; hence, decreased cox-2 activity may play a role in the remarkably low mortality from "Western" cancers enjoyed by Third World cultures in which systemic growth factor activity was minimized by quasi-vegan diets complemented by leanness and excellent muscle insulin sensitivity. Practical strategies for achieving a modest degree of calorie restriction may also have potential for down-regulating cox-2 expression while decreasing cancer risk. Soy isoflavones, linked to reduced cancer risk in Asian epidemiology, may suppress cox-2 induction by activating ERbeta. In aggregate, these considerations suggest that a comprehensive lifestyle strategy targeting cox-2 expression and bioactivity may have tremendous potential for cancer prevention.

Полный спектр антиоксидантной терапии, в числе астаксантин в сочетании с lipoprivic стратегий и salsalate для управления неалкогольной жировой болезни печени.

Благодаря Всемирной эпидемии ожирения, и популярность диет с высоким содержанием сахара и насыщенных жиров, неалкогольная жировая болезнь печени (НАЖБП) является более распространенным; это обычно связано с сопротивлением инсулина, и может рассматриваться как компонент метаболического синдрома. Патологий, которые могут осложнить стеатоз печени - стеатогепатит, цирроз и рак печени--появляются в результате взаимодействия печеночных липидов перегрузки печени и окислительного стресса. В связи с этим предлагается комплексный режимов, эффективно воздействует на каждый из этих провоцирующих факторов следует добиться наилучшего терапевтического эффекта в НАЖБП. Соответствующие потери веса, и диета с низким содержанием насыщенных жиров и низким гликемическим индексом, и добавлен сахар, следует уменьшить печени жировой нагрузки. Меры, которые повышают чувствительность к инсулину адипоцитов, такие как пиоглитазон, астаксантин, и спирулина--может также быть полезным в этом отношении, как могут агенты, которые повышают гепатоцитов емкость для окисления жирных кислот, таких как метформин, карнитин, гидроксицитрат, длинноцепочечные Омега-3 жиры, и глицин. Астаксантин и спирулину по-видимому значительный потенциал для управления окислительный стресс ассоциирован с НАЖБП - бывшей, потому что она может помочь предотвратить митохондриальные повреждения, делая митохондрий является основным источником супероксида при этом синдроме, второе, потому что это исключительно богат phycocyanobilin, в фитохимических NAPDH ингибитор оксидазы. Другие антиоксиданты, которые показывают обещание в этот синдром включают высокие дозы фолиевой кислоты, липоевая кислота, мелатонин, N-ацетилцистеин, витамин Е, таурин. Наконец, лечение с salsalate, ингибитор IkappaB киназы-бета, имеет потенциал для притупления неблагоприятное влияние стеатоза печени на окислительный стресс и воспаление.



Med Hypotheses. 2011 Oct;77(4):550-6. doi: 10.1016/j.mehy.2011.06.029. Epub 2011 Jul 20.

Full-spectrum antioxidant therapy featuring astaxanthin coupled with lipoprivic strategies and salsalate for management of non-alcoholic fatty liver disease.


McCarty MF1.

  • 1NutriGuard Research, 1051 Hermes Ave., Encinitas, CA 92024, United States. markfmccarty@gmail.com

Abstract


Owing to the worldwide epidemic of obesity, and the popularity of diets rich in sugar and saturated fat, nonalcoholic fatty liver disease (NAFLD) is increasingly common; it is usually associated with insulin resistance, and may be considered a component of the metabolic syndrome. The pathologies which can complicate hepatic steatosis--steatohepatitis, cirrhosis, and hepatic cancer--appear to result from an interaction of hepatic lipid overload and hepatic oxidative stress. It is therefore proposed that comprehensive regimens which effectively target each of these precipitating factors should achieve the best therapeutic benefit in NAFLD. Appropriate weight loss, and a diet low in saturated fat, glycemic index, and added sugars, should decrease hepatic lipid load. Measures which enhance adipocyte insulin sensitivity--such as pioglitazone, astaxanthin, and spirulina--may also be helpful in this regard, as may agents that boost hepatocyte capacity for fatty acid oxidation, such as metformin, carnitine, hydroxycitrate, long-chain omega-3 fats, and glycine. Astaxanthin and spirulina appear to have considerable potential for controlling the oxidative stress associated with NAFLD - the former because it may help to prevent the mitochondrial damage that renders mitochondria a key source of superoxide in this syndrome, the latter because it is exceptionally rich in phycocyanobilin, a phytochemical inhibitor of NAPDH oxidase. Other antioxidants which show some promise in this syndrome include high-dose folate, lipoic acid, melatonin, N-acetylcysteine, vitamin E, and taurine. Finally, treatment with salsalate, an inhibitor of IkappaB kinase-beta, has potential for blunting the adverse impact of hepatic steatosis on oxidative stress and inflammation.





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