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Lycopene Protects Against Spontaneous Ovarian Cancer Formation in Laying Hens
Kazim Sahin,Engin Yenice,Mehmet Tuzcu,Cemal Orhan,Cengizhan Mizrak,Ibrahim H. Ozercan,Nurhan Sahin,Bahiddin Yilmaz,Birdal Bilir,Bulent Ozpolat,Omer Kucuk 대한암예방학회 2018 Journal of cancer prevention Vol.23 No.1
Background: Dietary intake of lycopene has been associated with a reduced risk of ovarian cancer, suggesting its chemopreventive potential against ovarian carcinogenesis. Lycopene’s molecular mechanisms of action in ovarian cancer have not been fully understood. Therefore, in the present study, we investigated the effects of lycopene on the ovarian cancer formation using the laying hen model, a biologically relevant animal model of spontaneous ovarian carcinogenesis due to high incidence rates similar to humans. Methods: In this study, a total of 150 laying hens at age of 102 weeks were randomized into groups of 50: a control group (0 mg of lycopene per kg of diet) and two treatment groups (200 mg or 400 mg of lycopene per kg of diet, or ~26 and 52 mg/d/hen, respectively). At the end of 12 months, blood, ovarian tissues and tumors were collected. Results: We observed that lycopene supplementation significantly reduced the overall ovarian tumor incidence (P < 0.01) as well as the number and the size of the tumors (P < 0.004 and P < 0.005, respectively). Lycopene also significantly decreased the rate of adenocarcinoma, including serous and mucinous subtypes (P < 0.006). Moreover, we also found that the serum level of oxidative stress marker malondialdehyde was significantly lower in lycopene-fed hens compared to control birds (P < 0.001). Molecular analysis of the ovarian tumors revealed that lycopene reduced the expression of NF-B while increasing the expression of nuclear factor erythroid 2 and its major target protein, heme oxygenase 1. In addition, lycopene supplementation decreased the expression of STAT3 by inducing the protein inhibitor of activated STAT3 expression in the ovarian tissues. Conclusions: Taken together, our findings strongly support the potential of lycopene in the chemoprevention of ovarian cancer through antioxidant and anti-inflammatory mechanisms. (J Cancer Prev 2018;23:25-36)
( Matthew Sharp ),( Jacob Wilson ),( Matthew Stefan ),( Raad Gheith ),( Ryan Lowery ),( Charlie Ottinger ),( Dallen Reber ),( Cemal Orhan ),( Nurhan Sahin ),( Mehmet Tuzcu ),( Shane Durkee ),( Zainula 한국운동영양학회 2021 Physical Activity and Nutrition (Phys Act Nutr) Vol.25 No.1
[Purpose] This study investigated the effects of marine phytoplankton supplementation (Oceanix®, Tetraselmis chuii ) on 1) maximal isometric strength and immune function in healthy humans following a one-week high-intensity resistance-training program and 2) the proinflammatory cytokine response to exercise in a rat model. [Methods] In the human trial, 22 healthy male and female participants were randomly divided into marine phytoplankton and placebo groups. Following baseline testing, participants underwent a 14-day supplement loading phase before completing five consecutive days of intense resistance training. In the rat model, rats were randomly divided into four groups (n=7 per condition): (i) control, (ii) exercise, (iii) exercise + marine phytoplankton (2.55 mg/kg/day), or (iv) exercise + marine phytoplankton (5.1 mg/kg/day). Rats in the exercising groups performed treadmill exercise 5 days per week for 6 weeks. [Results] In the human model, marine phytoplankton prevented significant declines in the isometric peak rate of force development compared to placebo. Additionally, salivary immunoglobulin A concentration was significantly lower following the resistance training protocol in the placebo group but not in the marine phytoplankton group. Marine phytoplankton in exercising rats decreased intramuscular levels and serum concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) and intramuscular concentrations of malondialdehyde. [Conclusion] Marine phytoplankton prevented decrements in indices of functional exercise recovery and immune function. Mechanistically, these outcomes could be prompted by modulating the oxidative stress and proinflammatory cytokine response to exercise.