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Research Paper | November 21, 2022

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Suppression of isoproterenol induced apoptosis in H9c2 cardiomyoblasts cells by aescin

Kanimozhi Kaliyamoorthi, Tani Carmel Raj TG, Nivedha Jayaseelan, Sindhu Ganapathi, Vennila Lakshmanan

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Int. J. Biosci.21(5), 261-272, November 2022

DOI: http://dx.doi.org/10.12692/ijb/21.5.261-272

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Abstract

Medicinal herbs have been utilized for centuries to alleviate a spectrum of drugs. Horse chestnut (Aesculus hippocastanum) is used in phytomedicine to prevent and treat a wide range of conditions, and its seed extracts contain phytocompounds such as flavonoids, polyphenols, and triterpenoids (aescin). This study aims to investigate the potential mechanisms associated with the cardioprotective effect of aescin on isoproterenol (ISO) induced cardiotoxicity in H9c2 cell lines. The effect of the drug on cell morphology was studied by using a phase contrast microscope, and cell viability was studied by using 3-(4,5-dimethyl-thiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) staining, and reactive oxygen species (ROS) production was estimated by 20-7’dichlorofluorescein diacetate staining. H9c2 cells were treated with ISO to cause cell damage and the effect of the aescin on cell morphology, mitochondrial membrane potential, intracellular ROS generation, cell viability, and apoptosis was studied. The results of this study showed that pre-administration of aescin significantly reduced the ISO-induced toxic effects on cell morphology and enhanced the number of viable cells in a dose-dependent manner. This study also demonstrates that ROS generation was significantly increased in ISO-administered cells and ISO-induced ROS production was significantly reduced in the aescin-pre-administered H9c2 cells. ISO-induced changes in the mitochondrial membrane potential of H9c2 cells were remarkably improved with aescin pretreatment. These results clearly suggest that pretreatment of aescin protects the cells against ISO-induced damage by resuming mitochondrial function and regulating apoptosis.

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Suppression of isoproterenol induced apoptosis in H9c2 cardiomyoblasts cells by aescin

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