Abstract. Caffeic acid phenethyl ester (CAPE), a naturally occurring compound isolated from propolis extract, has been reported to have a number of biological and pharmacological properties, exerting antioxidant, anti-inflammatory, anticarcinogenic, antibacterial and immunomodulatory effects. Recent in vivo and in vitro study findings have provided novel insights into the molecular mechanisms involved in the anti-inflammatory and immunomodulatory activities of this natural compound. CAPE has been reported to have anti-inflammatory properties involving the inhibition of certain enzyme activities, such as xanthine oxidase, cyclooxygenase and nuclear factor-κB (NF-κB) activation. Since inflammation and immune mechanisms play a crucial role in the onset of several inflammatory diseases, the inhibition of NF-κB represents a rationale for the development of novel and safe anti-inflammatory agents. The primary goal of the present review is to highlight the anti-inflammatory and immunomodulatory activities of CAPE, and critically evaluate its potential therapeutic effects. Contents1. Introduction 2. Overview to the inflammatory response 3. Proinflammatory cytokines and signaling pathways 4. Anti-inflammatory effects of CAPE 5. Immunomodulatory effects of CAPE 6. Conclusion IntroductionCaffeic acid phenethyl ester (CAPE) is an important active component of honeybee propolis extract and has been used in traditional medicine for a number of years. CAPE is a polyphenol that contains hydroxyl groups within a catechol ring, the molecular formula of CAPE is C 17 H 16 O 4 (1,2) (Fig. 1). It has been shown that this active component of propolis possesses anti-inflammatory, immunomodulatory, antineoplastic, antioxidant and wound-healing properties (1-4). Inflammation is induced by the release of chemical mediators from damaged tissue and migratory cells. Mediators identified in the inflammatory process include biogenic amines, metabolites of arachidonic acid (eicosanoids), platelet aggregation factors, cytokines [interleukins (ILs) and tumor necrosis factor-α (TNF-α)] and free oxygen radicals. These substances are produced by inflammatory cells, such as polymorphonuclear leukocytes (neutrophils, eosinophils and basophils), endothelial cells, mast cells, macrophages, monocytes and lymphocytes (5,6). CAPE inhibits cytokine and chemokine production, the proliferation of T cells and lymphokine production, and thus suppresses the inflammatory process. Specifically, CAPE is a potent and a specific inhibitor of nuclear factor-κB (NF-κB) activation, and this may provide the molecular basis for its multiple anti-inflammatory and immunomodulatory activities (2,7). The aim of this review is to highlight the anti-inflammatory and immunomodulatory activities of CAPE, focusing on the mechanisms of action (already identified) underlying this activity. Overview to the inflammatory responseInflammation is an immunological response to pathogens and damage that is initiated to protect the body, and contributes Abbreviations: CAPE, caffeic acid phen...
Together with complex genetic and environmental factors, increased serum cholesterol and ox-LDL levels are considered as major triggering factors of atherosclerosis. Mononuclear cell infiltration to the arterial wall and uptake of ox-LDL, which is facilitated by CD36 receptor through an uncontrolled manner, play a key role in foam cell formation followed by atherogenesis development. The aim of this study was to analyze if CD36 expression in peripheral blood mononuclear cells reflect its aortic tissue level in hypercholesterolemia. In this study, CD36 protein expression was evaluated in aortic specimens of cholesterol or cholesterol plus Vitamin E treated animals in relation to the immunohistochemical analyses for the HNE-protein adducts, as well as for smooth muscle actin and vimentin. The CD36 mRNA expression was determined by RT-PCR in PBMC of hypercholesterolemic rabbits and hypercholesterolemic versus normocholesterolemic individuals. Immunohistochemistry findings revealed that smooth muscle actin, smooth muscle vimentin, HNE-protein conjugates, and CD36 protein expressions were significantly increased in aorta of hypercholesterolemic group where foam cells were present. High cholesterol diet significantly induced CD36 mRNA expression in both rabbit aorta and PBMCs, while positive correlation between aortic and PBMC CD36 expression has been found. In addition, consistent with the rabbit model, CD36 mRNA expression levels in human PBMCs were significantly higher in hypercholesterolemic patients than in normocholesterolemic individuals. Taken together, these results demonstrate that the CD36 mRNA levels of PBMCs could reflect the CD36 mRNA levels in aorta and could be used as a biomarker for diagnosis of atherosclerotic burden. © 2017 BioFactors, 2017.
Children with SK have increased 24-h urinary MA excretion in the long term, and need prolonged follow-up to detect early deterioration of renal function and to prevent end-organ damage later in life.
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