The Regulatory Effects of Magnolia Officinalis Extract on Aging-induced Mitochondrial Dysfunction in Cardiomyocytes
Abstract
Objectives: In this study, it is aimed to examine the protective effect of magnolia extract (ME), a herbal material obtained from Magnolia Officinalis,
which is claimed to have an important role in anti-inflammation, antioxidative stress and antiapoptosis, with increased reactive oxygen species
(ROS) production due to aging and depolarized mitochondrial membrane potential (MMP) in cardiomyocytes and its suppressive effect on apoptosis
and endoplasmic reticulum (ER) stress at the molecular level.
Materials and Methods: In the study, an in vitro aging model was created using rat left ventricular cell line H9c2. H9c2 cells treated with D-galactose
(D-Gal; 50 mg/mL) for 48 hours were incubated with 5 μM ME for 24 hours and their effects on ROS production and MMP depolarization in aged
cardiomyocytes were examined. ROS and MMP measurements were performed under confocal microscopy using fluorescent dyes dichlorofluorescin
diacetate (DCFDA) and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP). With the ER- stress markers Calregulin and glucose-regulated
protein 78, qRT-PCR measurements of the change in expression of the apoptosis marker equilibrative nucleoside transporter 1 after ME treatment
were analyzed.
Results: Incubation of aging-modeled cardiomyocytes with ME provides significant suppression of aging-related ROS production and regulation of
depolarized MMP. In addition, we observed that ER-stress and apoptosis developed by mitochondrial dysfunction were suppressed by ME treatment,
by examining the expressions of stress and apoptosis marker genes.
Conclusion: Our findings show that Magnolia officinalis extract, known for its cardioprotective effects, can be applied as a new treatment approach
in aging-related heart failure by regulating mitochondrion dysfunction that develops uncontrollably with cardiac aging at the functional and
molecular level.
Keywords
Aging, Magnolia Officinalis, Cardiomyocytes, ROS, Mitochondria, ER Stress, Apoptosis
Ethical Statement
Etik
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gerçekleştirilmiştir. İnsan ve hayvan deneyi içermemektedir. Bu
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Finansal Destek: Bu çalışma herhangi
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