Modified citrus pectin ameliorates myocardial fibrosis and inflammation via suppressing galectin-3 and TLR4/MyD88/NF-?B signaling pathway - 19/04/20
pages | 13 |
Iconographies | 11 |
Vidéos | 0 |
Autres | 0 |
Graphical abstract |
Highlights |
• | MCP ameliorates ISO-induced myocardial fibrosis and cardiac dysfunction. |
• | MCP decreases ISO-induced IL-1β, IL-18, TNF-α and Gal-3 levels. |
• | MCP ameliorates myocardial fibrosis via inhibiting TLR4/MyD88/NF-κB signaling. |
Abstract |
Myocardial fibrosis (MF) plays a key role in the development and progression of heart failure (HF) with limited effective therapies. Galectin-3 (Gal-3) is a biomarker associated with fibrosis and inflammation in patients with HF. The Gal-3 inhibitor modified citrus pectin (MCP) protects against cardiac dysfunction, though the underlying mechanism remains unclear. The aim of this study was to investigate the effect and mechanism of MCP on MF using an isoproterenol (ISO)-induced rat model of HF. Cardiac function was analyzed by echocardiography and electrocardiography. Histopathological changes in the heart tissue were assessed by hematoxylin-eosin and Masson trichrome staining. The mRNA and protein expression levels of signaling molecules and pro-inflammatory cytokines were monitored by immunohistochemistry, western blot, qRT-PCR and ELISA analyses. The results demonstrated that MCP ameliorated cardiac dysfunction, decreased myocardial injury and reduced collagen deposition. Furthermore, MCP downregulated the expression of Gal-3, TLR4 and MyD88, thereby inhibiting NF-κB-p65 activation. MCP also decreased the expression of IL-1β, IL-18 and TNF-α, which have been implicated in the pathogenesis of HF. These inhibitory effects were observed on day 15 and continued until day 22. Taken together, these results suggest that MCP ameliorates cardiac dysfunction through inhibiting inflammation and MF. These effects may be through downregulating Gal-3 expression and suppressing activation of the TLR4/MyD88/NF-κB signaling pathway. The present study supports the use of Gal-3 as a therapeutic target for the treatment of MF after myocardial infarction.
Le texte complet de cet article est disponible en PDF.Abbreviations : ANOVA, CO, ECG, ECM, EF, ELISA, FS, Gal-3, HE, HF, HFpEF, HFrEF, ISO, LPS, LV, LVEDD, LVESD, MCP, MF, MI, MR, RAAS, RIA, SD, SPI, SV
Keywords : Modified citrus pectin, Myocardial fibrosis, Heart failure, Galectin-3, TLR4, Inflammation
Plan
Vol 126
Article 110071- juin 2020 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’achat d’article à l’unité est indisponible à l’heure actuelle.
Déjà abonné à cette revue ?