NDLI: Apigenin ameliorates hypertension-induced cardiac hypertrophy and down-regulates cardiac hypoxia inducible factor-lα in rats

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Apigenin ameliorates hypertension-induced cardiac hypertrophy and down-regulates cardiac hypoxia inducible factor-lα in rats

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Food & Function Vol - 7 Issue - 3

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Apigenin ameliorates hypertension-induced cardiac hypertrophy and down-regulates cardiac hypoxia inducible factor-lα in rats

Content Provider	Royal Society of Chemistry (RSC)
Author	Huang, Yan Xie, Mei-Lin Zhu, Zeng-Yan Gao, Tian Xue, Jie
Copyright Year	2016
Abstract	Apigenin is a natural flavonoid compound that can inhibit hypoxia-inducible factor (HIF)-1α expression in cultured tumor cells under hypoxic conditions. Hypertension-induced cardiac hypertrophy is always accompanied by abnormal myocardial glucolipid metabolism due to an increase of HIF-1α. However, whether or not apigenin may ameliorate the cardiac hypertrophy and abnormal myocardial glucolipid metabolism remains unknown. This study aimed to examine the effects of apigenin. Rats with cardiac hypertrophy induced by renovascular hypertension were treated with apigenin 50–100 mg kg−1 (the doses can be achieved by pharmacological or dietary supplementation for an adult person) by gavage for 4 weeks. The results showed that after treatment with apigenin, the blood pressure, heart weight, heart weight index, cardiomyocyte cross-sectional area, serum angiotensin II, and serum and myocardial free fatty acids were reduced. It is important to note that apigenin decreased the expression level of myocardial HIF-1α protein. Moreover, apigenin simultaneously increased the expression levels of myocardial peroxisome proliferator-activated receptor (PPAR) α, carnitine palmitoyltransferase (CPT)-1, and pyruvate dehydrogenase kinase (PDK)-4 proteins and decreased the expression levels of myocardial PPARγ, glycerol-3-phosphate acyltransferase genes (GPAT), and glucose transporter (GLUT)-4 proteins. These findings demonstrated that apigenin could improve hypertensive cardiac hypertrophy and abnormal myocardial glucolipid metabolism in rats, and its mechanisms might be associated with the down-regulation of myocardial HIF-1α expression and, subsequently increasing the expressions of myocardial PPARα and its target genes CPT-1 and PDK-4, and decreasing the expressions of myocardial PPARγ and its target genes GPAT and GLUT-4.
Starting Page	1992
Ending Page	1998
Page Count	7
File Format	HTM / HTML PDF
ISSN	20426496
Volume Number	7
Issue Number	4
Journal	Food & Function
DOI	10.1039/c5fo01464f
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Apigenin Flavonoid Hypoxia-inducible factors Ventricular hypertrophy Cardiac muscle Metabolism Renovascular hypertension Force-feeding Cardiac muscle cell Angiotensin Protein Peroxisome Cell surface receptor Peroxisome proliferator-activated receptor Carnitine Pyruvate dehydrogenase kinase Peroxisome proliferator-activated receptor gamma Glycerol Phosphorylation Acyltransferase Glucose transporter Peroxisome proliferator-activated receptor alpha Carnitine palmitoyltransferase I GLUT4
Content Type	Text
Resource Type	Article
Subject	Medicine Food Science

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