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A Modified Simple Method for Induction of Myocardial Infarction in Mice
Published on: December 3, 2021
Cardioprotective Effects of Cuminaldehyde Mitigate Isoproterenol-Induced Myocardial Infarction by Modulating the
Shervin Prince Stanely1, Reya Issac1
1Division of Biotechnology, Karunya Institute of Technology and Sciences, Deemed to be University, Coimbatore, Tamil Nadu South, India.
Abstract:
Mitochondrial and endothelial dysfunction play a crucial role in the progression of myocardial infarction(MI). In this study, we appraised the cardioprotective effects of cuminaldehyde, a monocyclic terpenoid, and its molecular mechanisms by analyzing novel peroxisome proliferator-activated receptor-gamma coactivator-1α(PGC-1α)/NADH-dehydrogenase 2 (ND2)-mediated mitochondrial and endothelial nitric oxide synthase (eNOS)/nitric oxide (NO)/vascular cell adhesion molecule-1(VCAM-1) mediated endothelial dysfunction pathways in isoproterenol-induced myocardial infarcted rats. MI was induced in rats by isoproterenol (100 mg/kg body weight). Then, cuminaldehyde (20 mg/kg body weight) was administered orally daily for 3 weeks, and parameters related to mitochondrial and endothelial dysfunction were evaluated. The findings of this study showed that after isoproterenol administration, serum cardiac sensitive markers and heart rate increased. Furthermore, lipid peroxidation products and calcium ions were elevated, whereas antioxidants, isocitrate dehydrogenase, malate dehydrogenase, α-ketoglutarate dehydrogenase, NADH dehydrogenase, cytochrome c oxidase and adenosine triphosphate were decreased in isoproterenol-induced heart mitochondria. The transmission electron microscopic study validated mitochondrial damage. RT-PCR revealed reduced myocardial expression of PGC-1α and ND2. Moreover, the MI group showed lowered plasma NO, and the ELISA study revealed reduced eNOS and enhanced VCAM-1 in serum. The myocardial eNOS expression was diminished, and myocardial VCAM-1 expression was increased by RT-PCR. Histopathological findings revealed myocardial damage. Nevertheless, cuminaldehyde decreased cardiac diagnostic markers, heart rate, lipid peroxidation products, calcium ions, VCAM-1, and increased antioxidant system, mitochondrial enzymes, adenosine triphosphate, PGC-1α, ND2, NO, eNOS, and preserved mitochondrial and heart tissue architecture. Thus, cuminaldehyde modulated PGC-1α/ND2 and eNOS/NO/VCAM-1 pathways and alleviated mitochondrial and endothelial dysfunction, thereby mitigating MI in isoproterenol-induced rats and protecting the heart, by its anti-mitochondrial and anti-endothelial dysfunction mechanisms.
Insights
Cuminaldehyde protects against myocardial infarction by improving mitochondrial function and reducing endothelial dysfunction. It modulates key pathways, mitigating heart damage in a rat model.
Area of Science:
- Cardiovascular Pharmacology
- Mitochondrial Biology
- Endothelial Function
Background:
- Mitochondrial and endothelial dysfunction are key drivers of myocardial infarction (MI) progression.
- Understanding the molecular mechanisms underlying MI is crucial for developing effective treatments.
- Peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) and nitric oxide synthase (eNOS) pathways are implicated in cardiac health.
Purpose of the Study:
- To evaluate the cardioprotective effects of cuminaldehyde in a rat model of isoproterenol-induced myocardial infarction.
- To investigate the molecular mechanisms of cuminaldehyde involving PGC-1α/NADH-dehydrogenase 2 (ND2) and eNOS/nitric oxide (NO)/vascular cell adhesion molecule-1 (VCAM-1) pathways.
Main Methods:
- Myocardial infarction was induced in rats using isoproterenol.
- Cuminaldehyde was administered orally for three weeks.
- Evaluated cardiac markers, mitochondrial function, oxidative stress, PGC-1α/ND2 expression, and eNOS/NO/VCAM-1 pathway components using biochemical assays, RT-PCR, ELISA, and electron microscopy.
Main Results:
- Cuminaldehyde treatment significantly reduced cardiac markers, heart rate, lipid peroxidation, and calcium ions in MI rats.
- It restored mitochondrial enzyme activity, antioxidant levels, and adenosine triphosphate (ATP) production.
- Cuminaldehyde upregulated myocardial PGC-1α and ND2 expression, increased plasma NO and eNOS, and decreased VCAM-1 levels.
Conclusions:
- Cuminaldehyde exhibits significant cardioprotective effects against isoproterenol-induced myocardial infarction in rats.
- These benefits are mediated by modulating the PGC-1α/ND2 mitochondrial pathway and the eNOS/NO/VCAM-1 endothelial pathway.
- Cuminaldehyde preserves cardiac tissue architecture and function, highlighting its therapeutic potential for MI.
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