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Cardiac Oxidative Stress and Inflammation are Similar in SAMP8 and SAMR1 Mice and Unaltered by Curcumin and Ginkgo biloba Extract Intake

氧化应激 促炎细胞因子 衰老 谷胱甘肽 银杏 炎症 姜黄素 内分泌学 肿瘤坏死因子α 内科学 抗氧化剂 化学 医学 药理学 生物化学
作者
Christina Schiborr,Gunter P. Eckert,Jakob Weissenberger,Walter E. Muller,Dorothea Schwamm,Tilman Grune,Gerald Rimbach,Jan Frank
出处
期刊:Current Pharmaceutical Biotechnology [Bentham Science Publishers]
卷期号:11 (8): 861-867 被引量:14
标识
DOI:10.2174/138920110793262006
摘要

Chronic inflammation and oxidative stress increase with advancing age and appear to be involved in the pathogenesis of coronary heart disease, the leading cause of death worldwide. There is a need for animal models that reflect the increases in pro-inflammatory cytokines and oxidative damage observed during aging in humans. We therefore aimed to investigate the suitability of the fast-aging senescence-accelerated mouse-prone 8 (SAMP8) strain and its normally aging control senescence-accelerated mouse-resistant 1 (SAMR1) to study the age-dependent changes in cytokines, oxidative damage and antioxidants in the heart. To this end, 2-months-old male SAMR1 and SAMP8 mice were fed a Western type diet (control groups) for 5 months. Two groups of SAMP8 mice were simultaneously fed identical diets fortified with 0.5 g curcumin or 1.0 g Ginkgo biloba extract EGb 761® per kg diet. Heart tissue homogenates were analysed for protein carbonyls, glutathione, glutathione disulfide, methionine, cysteine and uric acid as well as the cytokines tumor-necrosis factor- α, interleukin-1β, interleukin-6, and monocyte chemoattractant protein-1. Neither the strain (SAMR1 or SAMP8) nor antioxidant intake (curcumin or EGb 761®) affected the concentrations of the measured parameters. In conclusion, our data do not support the suitability of the SAMP8 and SAMR1 strains as a model to study age-related changes in proinflammatory cytokines and oxidative stress parameters in the heart. Keywords: Aging, antioxidants, curcumin, Ginkgo biloba extract, heart health, inflammation, oxidative stress, senescenceaccelerated mice, cytokines, senescence-accelerated mouse-prone 8 (SAMP8), senescence-accelerated mouse-resistant 1 (SAMR1), protein carbonyls, glutathione, glutathione disulfide, methionine, cysteine, uric acid, tumor-necrosis factor-a, interleukin-1b, interleukin-6, Chronic inflammation, coronary heart disease (CHD), Curcuma longa, terpenelactones, flavonols quercetin, isorhamnetin, kaempferol, phytomedicine, Tissue Homogenates, phosphate-buffered saline, Protein Carbonyls, sulfuric acid, hemocyanin, streptavidin-biotinylated, Enzyme-Linked Immunosorbent Assay (ELISA), Glutathione disulfide, metaphosphoric acid, acetonitrile, isocratic elution, orthophosphoric acid, hydrophilic polypropylene, pathogenesis, atherosclerosis, Thiobarbituric acid reactive substances (TBARS)
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