Prevention of cardiovascular disease through nutritional supplements is growing in popularity throughout the world. Multiple epidemiologic studies found that moderate consumption of alcohol, particularly red wine, lowers mortality rates from coronary heart diseases (CHD). Chronic inflammation and atherosclerosis associated with CHD culminate in aberrant intravascular expression of tissue factor (TF), which triggers blood coagulation leading to thrombosis, a major cause for heart attack. We showed earlier that two red wine phenolics, resveratrol and quercetin, suppressed TF induction in endothelial cells. In the present study, we investigated efficacy of seven resveratrol derivatives, which were shown to be effective in regulating cancer cell growth in vitro at much lower concentrations than the parent compound resveratrol, in inhibiting TF induction in peripheral blood mononuclear cells (PBMCs). We also tested possible synergistic effects of resveratrol and quercetin with the other major red wine phenolics in suppression of lipopolysaccharide-induced TF expression in human PBMCs. We found that several resveratrol derivatives were 2- to 10-fold more efficient than resveratrol in inhibiting TF induction. Our study found no evidence for synergism among red wine polyphenolics. These data suggest that structural alterations of resveratrol can be effective in producing potent antithrombotic agents that will have therapeutic potential in the improvement of cardiovascular health and prevention of CHD. Among major red wine phenolics, quercetin appears to be the predominant suppressor of TF induction.
The currently available chemotherapeutic regimens against gastric cancer are not very effective, leading to high recurrence and poor survival. Resveratrol is a naturally occurring polyphenol with potent apoptosis-inducing activity. However, the mechanism underlying its actions remains unknown. In the present study, human gastric adenocarcinoma SGC7901 cells were treated with resveratrol (0, 25, 50, 100 and 200 ÎĽmol/L) for 48 h, and cellular apoptosis DNA damage were determined. In certain experiments, cells were incubated with superoxide dismutase (100 U/mL), catalase (300 U/mL) or sirtinol (10 ÎĽmol/L) to determine the role of reactive oxygen species (ROS) and sirtuin1 in resveratrol-induced cellular apoptosis. Treatment with resveratrol (50-200 ÎĽmol/L) for 48 h significantly induced apoptosis and DNA damage in human gastric cancer SGC7901 cells. This was due to the increased generation of ROS following resveratrol treatment because incubation of cells with superoxide dismutase (100 U/mL) or catalase (300 U/mL) attenuated resveratrol-induced cellular apoptosis. Interestingly, treatment with resveratrol (25-200 ÎĽmol/L) did not affect the level and activity of sirtuin1, whereas the sirtuin1 inhibitor sirtinol (10 ÎĽmol/L) significantly reduced sirtuin1 activity. Furthermore, treatment with sirtinol (10 ÎĽmol/L) did not have any effect on apoptosis induced by resveratrol. These data provide evidence that resveratrol induces apoptosis via ROS, but independent of sirtuin1, in the human gastric cancer cell line SGC7901.
Resveratrol in high doses has been shown to extend lifespan in some studies in invertebrates and to prevent early mortality in mice fed a high-fat diet. We fed mice from middle age (14-months) to old age (30-months) either a control diet, a low dose of resveratrol (4.9 mg kg(-1) day(-1)), or a calorie restricted (CR) diet and examined genome-wide transcriptional profiles. We report a striking transcriptional overlap of CR and resveratrol in heart, skeletal muscle and brain. Both dietary interventions inhibit gene expression profiles associated with cardiac and skeletal muscle aging, and prevent age-related cardiac dysfunction. Dietary resveratrol also mimics the effects of CR in insulin mediated glucose uptake in muscle. Gene expression profiling suggests that both CR and resveratrol may retard some aspects of aging through alterations in chromatin structure and transcription. Resveratrol, at doses that can be readily achieved in humans, fulfills the definition of a dietary compound that mimics some aspects of CR.
Prevention of malignant diseases, improvement of the quality of life of patients under cancer treatment regimens, care and rehabilitation. Observation of clinical status, changes in the course of the disease with emphasis on the quality of life during the use of the high bioflavonoid content Flavin7Â® dietary supplement.
Dietary supplement, Flavin7Â® was added to standard treatments, randomized,multi-center, controlled clinical trial on 295 patients in 33 centers.
Flavin7Â® is a dietary supplement containing bioflavonoid, resveratrol, anthocyanides, vitamins, minerals and trace-minerals. Its oxidative radical scavenging activity is a function of concentration and time, and exceeds the effectiveness of similar products on the market. In this study, the treating physicians found that Flavin7Â® inhibits the growth of tumours, reduces or alleviates the side effects of chemotherapy and radiation therapy. Flavin7Â® displays hepatoprotective properties and protects against cardio toxicity. Reduces pain caused by bone metastases. The treating physicians observed improved quality of life and symptoms of depression.
The review of international scientific literature and epidemiology data suggest that the role of bioflavonoids is more accepted in prevention. Presently, the scientifically proven treatment methods are not successful to reasonably improve quality of life, survival figures, complete and partial remission. Flavin7Â® given as a dietary supplement markedly improved the quality of life and the ratio of complete and partial remission of our patients. Our clinical observations suggest that the introduction of bioflavonoid supplements can effectively reduce the cardiovascular and cancer morbidity, mortality and chemo-prevention could become more successful. We strongly suggest further clinical research that meets the expectations and international standards of the society of oncologists. In the challenging field of oncology there is a place for complementary modalities of chemo-prevention and symptom-control.
A szĂv- Ă©s Ă©rrendszeri megbetegedĂ©sek tĂˇplĂˇlĂ©k kiegĂ©szĂtĹ‘k Ăˇltal tĂ¶rtĂ©nĹ‘ megelĹ‘zĂ©sĂ©nek nĂ©pszerĹ±sĂ©ge szerte a vilĂˇgon nĂ¶vekszik. TĂ¶bb epidemiolĂłgiai tanulmĂˇnyban is Ăşgy lĂˇttĂˇk, hogy a mĂ©rsĂ©kelt alkoholfogyasztĂˇs, kĂĽlĂ¶nĂ¶sen a vĂ¶rĂ¶sborĂ©, csĂ¶kkenti a koszorĂşeres szĂvbetegsĂ©gek [CHD â€“ coronary heart disease] esetĂ©ben a halĂˇlozĂˇsi arĂˇnyt. A CHD-vel kapcsolatos krĂłnikus gyulladĂˇs Ă©s Ă©relmeszesedĂ©s [atherosclerosis] a szĂ¶veti faktor [TF â€“ tissue factor, a subendotheĂˇlis szĂ¶vetekben talĂˇlhatĂł fehĂ©rje] rendellenes Ă©ren belĂĽli [intravaszkulĂˇris] kifejezĹ‘dĂ©sĂ©ben tetĹ‘zĹ‘dik, amely vĂ©rrĂ¶gkĂ©pzĹ‘dĂ©st indĂt el, ami trombĂłzishoz, a szĂvinfarktus fĹ‘ okĂˇhoz vezet. KorĂˇbban mĂˇr kimutattuk, hogy kĂ©t vĂ¶rĂ¶sbor fenol, a resveratrol Ă©s a quercetin elnyomja a TF indukciĂłt az Ă©r belsĹ‘ falĂˇt alkotĂł vĂ©kony sejtekben, az endotheliĂˇlis sejtekben. A jelen kutatĂˇsban hĂ©t olyan resveratrol szĂˇrmazĂ©k hatĂ©konysĂˇgĂˇt vizsgĂˇltuk a TF indukciĂł gĂˇtlĂˇsĂˇt tekintve a periferiĂˇlis vĂ©r mononukleĂˇris sejteknĂ©l [PBMC â€“ peripheral blood mononuclear cell], amelyek in vitro hatĂˇsosak voltak a rĂˇkos sejtnĂ¶vekedĂ©s szabĂˇlyozĂˇsĂˇban sokkal alacsonyabb koncentrĂˇciĂłkban, mint az eredeti resveratrol vegyĂĽletben. VizsgĂˇltuk a resveratrol Ă©s a quercetin lehetsĂ©ges szinergisztikus [egyĂĽtthatĂł] hatĂˇsait a tĂ¶bbi fĹ‘ vĂ¶rĂ¶sbor fenolokkal egyĂĽtt a lipopolysaccharid [zsĂr polisaccharid] indukĂˇlta TF kifejezĹ‘dĂ©sek gĂˇtlĂˇsĂˇban az emberi PBMC-kben. Azt talĂˇltuk, hogy szĂˇmos resveratrol szĂˇrmazĂ©k 2-10-szer hatĂ©konyabb volt, mint a resveratrol a TF indukciĂł gĂˇtlĂˇsĂˇban. KutatĂˇsunk nem talĂˇlt bizonyĂtĂ©kot szinergizmusra [amikor kĂ©t egyĂĽtthatĂł kombinĂˇciĂłja erĹ‘sebb, mint az egyĂĽtthatĂłk egyenkĂ©nt] a vĂ¶rĂ¶s bor poliphenolok kĂ¶zĂ¶tt. Ezek az adatok azt sugalljĂˇk, hogy a resveratrol szerkezeti ĂˇtalakĂtĂˇsai hatĂˇsosak lehetnek olyan hatĂ©kony trombĂłzis ellenes hatĂłanyagok elĹ‘ĂˇllĂtĂˇsĂˇban, amelyek gyĂłgyĂˇszati potenciĂˇllal rendelkeznek a szĂv- Ă©s Ă©rrendszeri egĂ©szsĂ©g javĂtĂˇsĂˇban Ă©s a CHD megelĹ‘zĂ©sĂ©ben. A fĹ‘bb vĂ¶rĂ¶s bor fenolok kĂ¶zĂĽl a quercetin tĹ±nik a TF indukciĂł dĂ¶ntĹ‘ elnyomĂłjĂˇnak.