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Published on: April 30, 2020
Ghrelin attenuates depressive-like behavior, heart failure, and neuroinflammation in postmyocardial infarction rat
Nan Sun1, Yong Mei1, Zhengtao Hu2
1Department of Gerontology, First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu, 241001, PR China; Key Laboratory of Non-coding RNA Transformation Research of Anhui Higher Education Institution (First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu, Anhui, 241001, PR China.
Insights
Ghrelin treatment improved cardiac function and reduced depression-like behaviors in rats with myocardial infarction (MI) and chronic heart failure (CHF). This suggests ghrelin may be a novel therapy for heart failure-associated depression.
Area of Science:
- Cardiovascular Medicine
- Neuroscience
- Pharmacology
Background:
- Depression is common after myocardial infarction (MI) and chronic heart failure (CHF), often resisting standard antidepressant treatments.
- Ghrelin, a peptide hormone, exhibits protective effects on both the heart and brain.
- The potential of ghrelin to alleviate depression following MI remains unexplored.
Purpose of the Study:
- To investigate whether ghrelin administration can attenuate depression-like behaviors in a rat model of MI and CHF.
- To evaluate the effects of ghrelin on cardiac function, neuroinflammation, and specific brain regions.
Main Methods:
- Myocardial infarction and chronic heart failure were induced in rats via coronary artery occlusion.
- Rats received subcutaneous injections of ghrelin (100 μg/kg) or vehicle twice daily for 4 weeks.
- Cardiac function, infarct size, cardiac remodeling, neuroinflammation markers (cytokines, microglial activation), and depression-like behaviors (sucrose preference, elevated plus maze, open field tests) were assessed.
Main Results:
- Ghrelin treatment significantly improved cardiac dysfunction, reduced infarct size, and mitigated cardiac remodeling.
- Ghrelin modulated inflammatory cytokine release and reduced microglial and astrocyte activation in the hippocampus (CA1 area).
- Behavioral assessments showed ghrelin administration markedly increased sucrose preference and locomotion, indicating reduced depression-like behavior.
Conclusions:
- Peripheral ghrelin administration demonstrates efficacy in inhibiting depression-like behavior and neuroinflammation in a rat model of CHF-associated depression.
- Ghrelin shows potential as a novel therapeutic strategy for treating depression in patients with chronic heart failure.
- These findings highlight the dual cardioprotective and neuroprotective roles of ghrelin in cardiovascular disease contexts.
Abstract:
Depression after myocardial infarction (MI) and chronic heart failure (CHF) is a common condition that is resistant to anti-depressive drugs. Ghrelin (a peptide hormone) shows dual protective effects on heart and brain. Whether ghrelin treatment attenuated depression after MI was investigated. Coronary artery occlusion was performed to induce MI and subsequent CHF in rats. Ghrelin (100 μg/kg in 0.5 ml of saline) or vehicle (0.5 ml of saline) was injected subcutaneously twice a day for 4 weeks. At week 5, all the animals underwent behavioral assessments including sucrose preference test (SPT), elevated plus maze test (EPM), and open field test (OFT). After cardiac function analysis, brain tissues were processed to determine inflammatory cytokines and microglial activations in hippocampus. Results showed that ghrelin substantially improved cardiac dysfunction, infarction size, and cardiac remodeling and modulated the release of inflammatory cytokines and the increase of Iba-1 positive microglia and glial fibrillary acidic protein-positive astrocytes in the CA1 area of hippocampus. Behavioral tests revealed that this treatment remarkably increased sucrose preference and mobile times and numbers. These findings provided evidence that peripheral ghrelin administration inhibits depression-like behavior and neuroinflammation and thus could be a new approach for the treatment of CHF-associated depression.
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