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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.