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Ursodeoxycholic acid impairs atherogenesis and promotes plaque regression by cholesterol crystal dissolution in mice.
Bode, Niklas; Grebe, Alena; Kerksiek, Anja; Lütjohann, Dieter; Werner, Nikos; Nickenig, Georg; Latz, Eicke; Zimmer, Sebastian.
Afiliação
  • Bode N; Medizinische Klinik und Poliklinik II, University Hospitals Bonn, 53105 Bonn, Germany.
  • Grebe A; Institute of Innate Immunity, University Hospitals Bonn, 53127 Bonn, Germany.
  • Kerksiek A; Institute of Clinical Chemistry und Clinical Pharmacology, University Hospitals Bonn, 53105 Bonn, Germany.
  • Lütjohann D; Institute of Clinical Chemistry und Clinical Pharmacology, University Hospitals Bonn, 53105 Bonn, Germany.
  • Werner N; Medizinische Klinik und Poliklinik II, University Hospitals Bonn, 53105 Bonn, Germany.
  • Nickenig G; Medizinische Klinik und Poliklinik II, University Hospitals Bonn, 53105 Bonn, Germany.
  • Latz E; Institute of Innate Immunity, University Hospitals Bonn, 53127 Bonn, Germany; Department of Infectious Diseases and Immunology, UMass Medical School, Worcester, MA 01605, USA; German Center of Neurodegenerative Diseases (DZNE), 53127 Bonn, Germany.
  • Zimmer S; Medizinische Klinik und Poliklinik II, University Hospitals Bonn, 53105 Bonn, Germany. Electronic address: sebastian.zimmer@ukb.uni-bonn.de.
Biochem Biophys Res Commun ; 478(1): 356-362, 2016 09 09.
Article em En | MEDLINE | ID: mdl-27416761
Atherosclerosis is a chronic inflammatory disease driven primarily by a continuous retention of cholesterol within the subendothelial space where it precipitates to form cholesterol crystals (CC). These CC trigger a complex inflammatory response through activation of the NLRP3 inflammasome and promote lesion development. Here we examined whether increasing cholesterol solubility with ursodeoxycholic acid (UDCA) affects vascular CC formation and ultimately atherosclerotic lesion development. UDCA mediated intracellular CC dissolution in macrophages and reduced IL-1ß production. In ApoE(-/-) mice, UDCA treatment not only impaired atherosclerotic plaque development but also mediated regression of established vascular lesions. Importantly, mice treated with UDCA had decreased CC-depositions in atherosclerotic plaques compared to controls. Together, our data demonstrate that UDCA impaired CC and NLRP3 dependent inflammation by increasing cholesterol solubility and diminished atherosclerosis in mice.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Ursodesoxicólico / Colesterol / Aterosclerose / Placa Aterosclerótica Limite: Animals Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Alemanha

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Ursodesoxicólico / Colesterol / Aterosclerose / Placa Aterosclerótica Limite: Animals Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Alemanha