IParkia speciosa/I Hassk. Empty Pod Extract Prevents Cardiomyocyte Hypertrophy by Inhibiting MAPK and Calcineurin-NFATC3 Signaling Pathways

Cardiac hypertrophy is an early hallmark during the clinical course of heart failure. Therapeutic strategies aiming to alleviate cardiac hypertrophy via the mitogen-activated protein kinase (MAPK)/calcineurin-nuclear factor of activated T-cells (NFAT) signaling pathway may help prevent cardiac dysfu...

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Bibliographic Details
Published in:Life (Basel, Switzerland) Switzerland), 2022-12, Vol.13 (1)
Main Authors: Mustafa, Nor Hidayah, Jalil, Juriyati, Saleh, Mohammed S. M, Zainalabidin, Satirah, Asmadi, Ahmad Yusof, Kamisah, Yusof
Format: Article
Language:English
Subjects:
Acetates
Alcohol industry
Beans
Calcineurin
Cellular proteins
Cellular signal transduction
Esters
Health aspects
Heart
Heart cells
Heart enlargement
Instrument industry
Legumes
Medicinal plants
Mimosaceae
Mitogen-activated protein kinases
Natriuretic peptides
Oxidases
Prevention
Protein binding
Protein kinases
T cells
Valsartan
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Summary:Cardiac hypertrophy is an early hallmark during the clinical course of heart failure. Therapeutic strategies aiming to alleviate cardiac hypertrophy via the mitogen-activated protein kinase (MAPK)/calcineurin-nuclear factor of activated T-cells (NFAT) signaling pathway may help prevent cardiac dysfunction. Previously, empty pod ethanol crude extract of Parkia speciosa Hassk was shown to demonstrate protective effects against cardiomyocyte hypertrophy. Therefore, the current study aimed to investigate the effects of various fractions of the plant ethanol extract on the MAPK/NFAT signaling pathway in angiotensin II (Ang II)-induced cardiomyocyte hypertrophy. Simultaneous treatment with ethyl acetate (EA) fraction produced the most potent antihypertrophic effect evidenced by the reduced release of B-type natriuretic peptide (BNP). Subsequently, treatment with the EA fraction (6.25, 12.5, and 25 μg/mL) prevented an Ang II-induced increase in cell surface area, hypertrophic factors (atrial natriuretic peptide and BNP), reactive oxygen species, protein content, and NADPH oxidase 4 expression in the cells. Furthermore, EA treatment attenuated the activation of the MAPK pathway and calcineurin-related pathway (GATA-binding protein 4 and NFATC3), which was similar to the effects of valsartan (positive control). Our findings indicate that the EA fraction prevents Ang II-induced cardiac hypertrophy by regulating the MAPK/calcineurin-NFAT signaling pathway.
ISSN:2075-1729
2075-1729
DOI:10.3390/life13010043