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Chwan-Li Shen,Jodie Peterson,Owatha L. Tatum,Dale M. Dunn 한국식품영양과학회 2008 Journal of medicinal food Vol.11 No.1
This study examined the effects of eicosapentaenoic acid (EPA) and arachidonic acid (AA) on inflammation mediators during osteoblastogenesis, in terms of modulation of the cyclooxygenase (COX)-2 and the inducible nitric oxide (NO) synthase (iNOS) pathways. We hypothesized that n-3 polyunsaturated fatty acid (PUFA) would reduce the production of inflammation mediators, including prostaglandin E2 (PGE2) and NO, and related mRNA gene expression during osteoblastogenesis. Mouse bone marrow stromal cells (ST-2) were treated with 40 M ethanol (as a control), 40 M AA, or 40 M EPA in osteogenic medium for 7, 14, 21, or 28 days. Prior to harvest, cells were treated with respective treatments along with cytokine mixtures for an additional 24 hours, and then cells were harvested for mRNA expression. In addition, cells were also treated with respective treatments along with the same cytokine mixtures for an additional 48 hours for experiment measuring PGE2 and NO production using conditioned culture medium and protein expression using cells. Except for 7 days of culture, AA treatment resulted in the highest value for PGE2 production throughout 28 days of culture. AA treatment also enhanced COX-2 mRNA expression up to 21 days. AA treatment resulted in a higher value for NO production after 7 days, while EPA treatment yielded a higher value for NO production relative to those receiving AA treatment after 14 and 21 days. Our investigation has corroborated that the protective action of EPA on osteoblastogensis was mediated by the modulation of PGE2 and the NO pathway.
Chwan-Li Shen,Christina Samathanam,Suzanne Graham,Raul Y. Dagda,Ming-Chien Chyu,Dale M. Dunn 한국식품영양과학회 2012 Journal of medicinal food Vol.15 No.3
Studies have suggested that 1-a-OH-vitamin D3 and green tea polyphenols (GTPs) are promising dietary supplements for mitigating chronic inflammation-induced fibrosis of vessels because of their anti-inflammatory properties. This study evaluated (1) the impact of 1-a-OH-vitamin D3 on myocardial fibrosis in female rats with chronic inflammation and (2) if 1-a-OH-vitamin D3 and GTPs have an additive or synergistic effect to attenuate myocardial fibrosis in these female rats. A 3-month study of a 2 (no 1-a-OH-vitamin D3 vs. 0.05 lg/kg 1-a-OH-vitamin D3, five times per week) · 2 (no GTPs vs. 0.5% GTPs in drinking water) factorial design in lipopolysaccharide (LPS)-administered female rats was performed. Additionally, a group receiving placebo administration was used to compare with a group receiving LPS administration only to evaluate the effect of LPS. Masson’s Trichrome staining evaluated myocardial fibrosis in coronary vessels and surrounding myocardium. Spleen cyclooxygenase-2 mRNA expression was determined by real-time polymerase chain reaction. Total lipid profiles were also determined. Whole blood was used for differential cell counts. Data were analyzed by two-way analysis of variance followed by mean separation procedures. At 3 months LPS administration induced myocardial fibrosis in vessels and surrounding myocardium, spleen cyclooxygenase-2 mRNA expression, and elevated leukocyte counts, whereas both 1-a-OHvitamin D3 administration and GTPs supplementation significantly attenuated these pro-inflammatory events. The inhibitory effects of 1-a-OH-vitamin D3 and GTPs seem to be an individual effect, instead of an additive or synergistic effect. 1-a-OHvitamin D3 and GTPs lowered red blood cell counts, hematocrit, and hemoglobin. Neither 1-a-OH-vitamin D3 nor GTPs affected lipid profiles. In summary, both 1-a-OH-vitamin D3 administration and GTPs supplementation mitigate myocardial fibrosis through suppression of a chronic inflammation innate immune response.