Keywords: Antiinflammatory Agent, Apolipoprotein A1, Cholesterol Ester, Haptoglobin, High Density Lipoprotein Cholesterol, Isoenzyme, Nitric Oxide Synthase, Peptide P2a, Prostaglandin E2, Prostaglandin Synthase, Unclassified Drug, Animal Experiment, Animal Model, Antiinflammatory Activity, Article, Cholesterol Blood Level, Cholesterol Esterification, Controlled Study, Drug Effect, Drug Mechanism, Enzyme Linked Immunosorbent Assay, High Performance Liquid Chromatography, In Vivo Study, Mouse, Nonhuman, Paw Edema, Priority Journal, Protein Binding, Protein Blood Level, Protein Expression, Protein Function, Western Blotting, Amino Acid Sequence, Anti-Inflammatory Agents, Cyclooxygenase 2, Dinoprostone, Dose-Response Relationship, Molecular Sequence Data, Phosphatidylcholine-Sterol O-Acyltransferase,
Affiliations: *** IBB - CNR ***
Department of Experimental Pharmacology, University of Naples Federico II, via Domenico Montesano 49, 80131 Naples, Italy.
Department of Biological Sciences, University of Naples Federico II, Naples, Italy
Biostructures and Bioimaging Institute, Consiglio Nazionale Delle Ricerche, Naples, Italy
References: Not available.
Apolipoprotein A-I (ApoA-I) mimetic peptide P2a by restoring cholesterol esterification unmasks ApoA-I anti-inflammatory endogenous activity in vivo
Santulli G, Cipolletta E, Sorriento D, Del Giudice C, Anastasio A, Monaco S, Maione AS, Condorelli G, Puca A, Trimarco B, Illario M, Iaccarino G * CaMK4 gene deletion induces hypertension(435 views) J Am Heart Assoc Journal Of The American Heart Association (ISSN: 2047-9980), 2012; 1(4): N/D-N/D. Impact Factor:2.882 ViewExport to BibTeXExport to EndNote