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Updated: Feb 1, 2026

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice
Published on: October 3, 2019
Nanoyttria attenuates isoproterenol-induced cardiac injury
Chandraiah Godugu1, Preeti Kumari1, Amit Khurana1
1Department of Regulatory Toxicology, National Institute of Pharmaceutical Education & Research (NIPER), Balanagar, Hyderabad, Telangana State, PIN-500037, India.
Aim:
The present study was designed to probe the cardioprotective effects of nanoyttria (NY).
Materials & Methods:
NY was characterized using various techniques. Isoproterenol (ISO)-induced cardiotoxicity challenged mice were treated with NY for 28 days at two doses (0.4 and 4 mg/kg, intraperitoneally).
Results:
NY demonstrated free radical scavenging activity as shown by a 2,2-diphenyl-1-picrylhydrazyl assay. NY treatment showed alleviation of ISO-induced cardiotoxicity as evident from the reduction in biochemical parameters. The expression of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) showed significant decrease upon NY treatment. Histopathology and ECG showed protection in histoarchitecture and rhythm of heart, respectively. Reduction in hydroxyproline and TGF-β1 expression indicated antifibrotic activity.
Conclusion:
We report for the first time that NY ameliorates ISO-induced cardiac remodeling.
Insights
Nanoyttria (NY) protects against isoproterenol-induced cardiotoxicity by reducing inflammation and fibrosis. This study shows NY ameliorates cardiac remodeling, offering potential therapeutic benefits for heart conditions.
Area of Science:
- Biomedical Engineering
- Materials Science
- Cardiology
Background:
- Isoproterenol (ISO) is widely used to induce cardiotoxicity in animal models.
- Cardiac remodeling is a pathological process that leads to heart failure.
- Nanomaterials are being explored for their therapeutic potential in cardiovascular diseases.
Purpose of the Study:
- To investigate the cardioprotective effects of nanoyttria (NY).
- To evaluate NY's efficacy in mitigating ISO-induced cardiotoxicity and cardiac remodeling.
Main Methods:
- Nanoyttria (NY) characterization using various techniques.
- Induction of cardiotoxicity in mice using Isoproterenol (ISO).
- Treatment of ISO-challenged mice with two doses of NY (0.4 and 4 mg/kg) for 28 days.
- Assessment of biochemical parameters, proinflammatory cytokines (IL-1β, IL-6, TNF-α), histopathology, ECG, hydroxyproline, and TGF-β1 expression.
Main Results:
- NY exhibited free radical scavenging activity.
- NY treatment alleviated ISO-induced cardiotoxicity, reducing key biochemical markers.
- Significant decrease in proinflammatory cytokines (IL-1β, IL-6, TNF-α) was observed.
- Histopathology and ECG confirmed protection of cardiac histoarchitecture and rhythm.
- Reduced hydroxyproline and TGF-β1 expression indicated antifibrotic activity of NY.
Conclusions:
- Nanoyttria (NY) demonstrates significant cardioprotective effects against ISO-induced cardiotoxicity.
- NY ameliorates cardiac remodeling by reducing inflammation and fibrosis.
- This study is the first to report NY's ability to mitigate ISO-induced cardiac remodeling, suggesting its therapeutic potential.
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