Your browser doesn't support javascript.
loading
Oleuropein prevents the development of experimental autoimmune myocarditis in rats.
Zhang, Jia-Ying; Yang, Zheng; Fang, Kun; Shi, Zhan-Li; Ren, Dan-Hong; Sun, Jing.
Affiliation
  • Zhang JY; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China.
  • Yang Z; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China.
  • Fang K; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China.
  • Shi ZL; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China.
  • Ren DH; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China.
  • Sun J; Department of Critical Care Medicine, Hang Zhou Red Cross Hospital, Hangzhou 310014, Zhejiang, China. Electronic address: sunjcross@163.com.
Int Immunopharmacol ; 48: 187-195, 2017 Jul.
Article de En | MEDLINE | ID: mdl-28525856
ABSTRACT
Oleuropein (OLE) is a natural secoiridoid that is derived from Olea europaea. OLE possesses cardioprotective effects in experimental models of hypertension, myocardial infarction, atherosclerosis and hyperlipidaemia. In the present study, the effects of OLE on experimental autoimmune myocarditis (EAM) were evaluated. EAM in rats were induced by subcutaneous injections of porcine cardiac myosin. Cardiac function parameters, myocardial pathology, myocardial inflammatory cell infiltration and nuclear factor kappa-B (NF-κB) expression were measured. Our data showed that the postmyocarditis rats exhibited increased left ventricular end systolic diameters, left ventricular end diastolic diameters, left ventricular end-diastolic pressures (LVEDP), and decreased ejection fractions. However, OLE significantly suppressed these changes in EAM rats. Histological analysis revealed that myosin induced miliary foci of discolouration on endocardial surfaces and extensive myocardial injuries with inflammatory cell infiltration were significantly improved by OLE therapy. A definitive positive correlation between the histological scores and LVEDP was observed. Moreover, OLE inhibited CD4+, CD8+ cells and macrophage infiltration in myocardium and decreased the serum production of tumour necrosis factor-a (TNF-a), interleukin-1ß (IL-1ß) and IL-6 in EAM rats. Expectedly, the myocardial levels of NF-κB p65, p-IκBa, IKKa were significantly attenuated by OLE, indicating the inhibitory effects of OLE on the NF-κB pathway. Furthermore, OLE decreased the myocardial expressions of phosphorylated-p38 MAPK, phosphorylated-ERK, and did not change the levels of p38 MAPK and ERK in EAM rats. Collectively, our results suggest that OLE effectively prevents the development of myocarditis, at least in part, by inhibiting the MAPKs and NF-κB mediated inflammatory responses.
Sujet(s)
Mots clés

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Maladies auto-immunes / Cardiotoniques / Iridoïdes / Myocardite Type d'étude: Prognostic_studies Limites: Animals Langue: En Journal: Int Immunopharmacol Sujet du journal: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Année: 2017 Type de document: Article Pays d'affiliation: Chine

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Maladies auto-immunes / Cardiotoniques / Iridoïdes / Myocardite Type d'étude: Prognostic_studies Limites: Animals Langue: En Journal: Int Immunopharmacol Sujet du journal: ALERGIA E IMUNOLOGIA / FARMACOLOGIA Année: 2017 Type de document: Article Pays d'affiliation: Chine