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Updated: May 15, 2026

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
Published on: October 3, 2019
Protective effect of neferine against isoproterenol-induced cardiac toxicity
Gurusamy Lalitha1, Paramasivan Poornima, Arjunan Archanah
1Animal Tissue Culture Laboratory, Department of Biotechnology, School of Biotechnology and Genetic Engineering, Bharathiar University, Coimbatore 641046, Tamilnadu, India.
Abstract:
The present study was designed to investigate the cardioprotective effect of neferine against isoproterenol-induced myocardial infarction. Neferine was given orally for 30 days, and isoproterenol was injected subcutaneously for 2 days. Histopathological examination of heart tissue of isoproterenol-treated rats showed myocardial necrosis. Biochemical analysis of isoproterenol-treated rats showed significant increase in the serum marker enzymes--creatine kinase, lactate dehydrogenase, and aspartate transaminase and increased serum glycoprotein components with a concomitant decrease in the heart tissue homogenate when compared to control. Increased lipid peroxidation and decreased antioxidants reduced glutathione, superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase and altered lipid profile in serum and tissue was also recorded in the isoproterenol-treated rats, whereas the rats which received neferine pre-treatment followed by isoproterenol injection showed minimal histological changes, absence of inflammation, and a significant decrease in the serum marker enzymes and serum glycoprotein components with a concomitant increase in the heart tissue homogenate when compared to isoproterenol group. Neferine pre-treatment restored the altered biochemical parameters and lipid profile to near normal. The results of the present study showed that neferine exerts strong antioxidant property against isoproterenol-induced oxidative stress and can be used as a potent cardioprotective agent against isoproterenol-induced myocardial infarction.
Insights
Neferine protects the heart against damage from isoproterenol-induced myocardial infarction by reducing oxidative stress. This study shows neferine is a potent cardioprotective agent, preserving heart tissue and restoring biochemical markers.
Area of Science:
- Pharmacology
- Cardiovascular Research
- Natural Product Chemistry
Background:
- Myocardial infarction (MI) is a leading cause of death worldwide.
- Isoproterenol (ISO) is commonly used to induce experimental MI in animal models.
- Oxidative stress plays a critical role in the pathogenesis of MI.
Purpose of the Study:
- To investigate the cardioprotective effects of neferine against ISO-induced MI.
- To evaluate the antioxidant properties of neferine in a cardiac injury model.
- To determine if neferine can mitigate biochemical and histological damage caused by ISO.
Main Methods:
- Rats were pre-treated with neferine orally for 30 days, followed by subcutaneous ISO injection for 2 days.
- Histopathological examination of heart tissues was performed.
- Serum and heart tissue homogenates were analyzed for marker enzymes, glycoprotein components, lipid peroxidation, antioxidants, and lipid profiles.
Main Results:
- ISO-induced rats exhibited myocardial necrosis, elevated serum marker enzymes (creatine kinase, lactate dehydrogenase, aspartate transaminase), increased serum glycoproteins, and decreased heart tissue glycoproteins.
- Increased lipid peroxidation and reduced antioxidant levels (glutathione, superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase) were observed in ISO-treated rats.
- Neferine pre-treatment significantly reduced histological damage, decreased serum marker enzymes and glycoproteins, and restored antioxidant levels and lipid profiles towards normal.
Conclusions:
- Neferine demonstrates significant cardioprotective effects against ISO-induced myocardial infarction.
- Neferine exerts potent antioxidant properties, mitigating ISO-induced oxidative stress.
- Neferine holds potential as a therapeutic agent for preventing or treating myocardial infarction.
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