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Effect of Naringin on Cardiac Toxicity, Hypertrophy, and Remodeling

Effect of Naringin on Cardiac Toxicity, Hypertrophy, and Remodeling.

Isoproterenol-induced myocardial infarction was prevented by naringin supplementation (40 mg · kg−1 · d−1) in rats . Naringin supplementation also reduced lipid peroxidation, improved antioxidant enzymes, and decreased inflammatory cell and fibrosis in hearts of isoproterenol-treated rats . Pretreatment with various doses of naringin inhibited the doxorubicin-induced decline in antioxidant status and reduced the concentrations of 8-OHdG and the activity of poly (ADP-ribose) polymerase (PARP) in heart and liver of mice. Oral pretreatment with naringin (10, 20, and 40 mg/kg) in isoproterenol-induced rats daily for a period of 56 d significantly (P < 0.05) minimized the alterations in mitochondrial tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and α-ketoglutarate dehydrogenase) and respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase).


A high-fat diet induces cardiac remodeling and fibrosis in experimental animals. In the early stage of fibrosis, massive inflammatory cells, mainly macrophages, infiltrate into the left ventricle of heart. This fibrosis starts from the vascular region of the heart muscle and then disseminates across the left ventricle. Chamber dilation and ballooning have also been observed due to high-fat-diet feeding. Further echocardiographic data confirmed the left ventricular dysfunction and increased left ventricular mass in high-fat/high-carbohydrate-diet–induced obese rats. Naringin supplementation in these rats improved the inflammatory state and fibrosis, which ultimately reduced the left ventricular stiffness constant . Moreover, naringin supplementation improved many of the left ventricular functional variables, such as percentage of fractional shortening, and prevented the cardiac remodeling in hearts of these rats . A recent study showed that naringin (60 and 120 mg/kg) significantly reduced paraquat-induced pulmonary fibrosis by downregulating TNF-α, TGF-β1, matrix metalloproteinase 9 (MMP-9), and tissue inhibitor of metalloproteinase 1 (TIMP-1), which are the key regulators of fibrosis in tissues. The mechanism of naringin-induced cardiomyocyte protection has been revealed recently. Naringin (5 μmol/L) attenuated high-glucose–induced (16.7 mmol/L) p38 and p53 phosphorylation, decreased mitochondrial Bax and Bak expression, prevented the release of cytochrome c, and increased Bcl-2 expression in H9c2 cells. Moreover, it also prevented high-glucose–induced apoptosis in H9c2 cells followed by inactivation of caspase-3, -8, and -9. In another study, naringin prevented cardiomyocytes due to high-glucose (35 mmol/L glucose) challenge followed by ROS-activated MAPK signal–mediated pathways. Naringin (80 μmol/L) prevented the high-glucose–induced phosphorylation of p38 MAPK, ERK1/2, and JNK and reduced apoptosis in H9c2 cardiac cells.

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