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Ghrelin prevents cardiac cell apoptosis during cardiac remodelling post experimentally induced myocardial infarction in rats via activation of Raf-MEK1/2-ERK1/2 signalling.
- Source :
- Archives of Physiology & Biochemistry; May2019, Vol. 125 Issue 2, p93-103, 11p
- Publication Year :
- 2019
-
Abstract
- Context: Mechanisms by which ghrelin affords its cardioprotection in mammals remained unclear. Objective: To examine if ghrelin confers cardio-protection during cardiac remodelling post-MI by modulating the RAF-1-MEK1/2-ERK1/2 signalling pathway. Materials and methods: Rats were divided into control, sham, sham + ghrelin, myocardial infarction (MI), and MI + ghrelin groups. Ghrelin (100 µg/kg) was administered for 21 days, starting one-day post-MI. Results: Ghrelin enhanced cardiac contractility and the activities of antioxidant enzymes, lowered serum levels of enzyme markers of cardiac dysfunction, and lowered inflammatory mediator levels. Ghrelin increased levels of phospho-Raf-1 (Ser<superscript>338</superscript>), phospho-MEK1/2 (Ser<superscript>217/221</superscript>), phospho-ERK1/2 (Thr<superscript>202</superscript>/Tyr<superscript>204</superscript>), and of their downstream target p-BAD (Ser<superscript>112</superscript>) and inhibited the cleavage of caspase-3. Concomitantly, ghrelin prevented the increases in the levels of fibrotic markers, including α-smooth muscle actin (α-SMA), metalloproteinase-9 (MPP-9), and type III collagen. Conclusion: Post-MI in rats, ghrelin stimulated Raf-1-MEK1/2-ERK1/2-BAD signalling in the LV infarct areas, accounting for its anti-apoptotic effect, enhancing cardiac function, and inhibiting cardiac fibrosis during cardiac remodelling. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 13813455
- Volume :
- 125
- Issue :
- 2
- Database :
- Complementary Index
- Journal :
- Archives of Physiology & Biochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 135567214
- Full Text :
- https://doi.org/10.1080/13813455.2018.1437751