title: Green tea polyphenols and 1-α-OH-vitamin D₃ attenuate chronic inflammation-induced myocardial fibrosis in female rats.
abstract: Studies have suggested that 1-α-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-α-OH-vitamin D₃ on myocardial fibrosis in female rats with chronic inflammation and (2) if 1-α-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-α-OH-vitamin D₃ vs. 0.05 μg/kg 1-α-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-α-OH-vitamin D₃ administration and GTPs supplementation significantly attenuated these pro-inflammatory events. The inhibitory effects of 1-α-OH-vitamin D₃ and GTPs seem to be an individual effect, instead of an additive or synergistic effect. 1-α-OH-vitamin D₃ and GTPs lowered red blood cell counts, hematocrit, and hemoglobin. Neither 1-α-OH-vitamin D₃ nor GTPs affected lipid profiles. In summary, both 1-α-OH-vitamin D₃ administration and GTPs supplementation mitigate myocardial fibrosis through suppression of a chronic inflammation innate immune response.
authors.affiliation: Department of Pathology, Texas Tech University Health Sciences Center, Lubbock, Texas, USA. leslie.shen@ttuhsc.edu
authors.forename: Chwan-Li
authors.initials: CL
authors.lastname: Shen
authors.forename: Christina
authors.initials: C
authors.lastname: Samathanam
authors.forename: Suzanne
authors.initials: S
authors.lastname: Graham
authors.forename: Raul Y
authors.initials: RY
authors.lastname: Dagda
authors.forename: Ming-Chien
authors.initials: MC
authors.lastname: Chyu
authors.forename: Dale M
authors.initials: DM
authors.lastname: Dunn
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D003331:Coronary Vessels / Q000276:immunology / Q000473:pathology; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D019587:Dietary Supplements; D004719:Endomyocardial Fibrosis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006887:Hydroxycholecalciferols / Q000627:therapeutic use*; D007113:Immunity, Innate; D007964:Leukocytosis / Q000276:immunology / Q000517:prevention & control; D009206:Myocardium / Q000276:immunology / Q000473:pathology; D008517:Phytotherapy; D059808:Polyphenols / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D011919:Rats, Inbred Strains; D013154:Spleen / Q000276:immunology / Q000378:metabolism; D013662:Tea / Q000737:chemistry*
chemical_list: D000893:Anti-Inflammatory Agents; D006887:Hydroxycholecalciferols; D059808:Polyphenols; D012333:RNA, Messenger; D013662:Tea; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; C008088:alfacalcidol