Rosuvastatin changes cytokine expressions in ischemic territory and preserves heart function after acute myocardial infarction in rats
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Updated: May 17, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Xinying Hu1, Aijun Sun, Xinxing Xie
1Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Aim:
To investigate the mechanism of rosuvastatin in preserving cardiac function after acute myocardial infarction (AMI) in a rat model.
Methods:
Sprague-Dawley rats were randomized to receive either rosuvastatin (5 mg/kg every day) or placebo (0.5% CMC-Na), respectively, by daily gavage from 7 days before AMI. Acute myocardial infarction (AMI) model was induced by left anterior descending coronary artery ligation through a lateral thoracotomy in rats. The expressions of stromal-cell-derived factor 1 (SDF-1), chemokine motif CXC receptor 4 (CXCR-4), vascular endothelial growth factor (VEGF), and intercellular adhesion molecule 1 (ICAM-1) in peri-infarction region and nonischemic region at different time points were determined by the Western blot analysis. Immunohistochemistry analysis was performed on the 28th day after AMI to investigate the accumulation of CD90+, CD133+, and c-kit+ progenitor cells in the peri-infarction region. Masson staining and echocardiograph were performed to evaluate the left ventricular remodeling and postinfarction cardiac function 4 weeks after AMI.
Results:
Western blot analysis showed that rosuvastatin could change the cytokine expressions in the peri-infarction region by upregulating the SDF-1 expression and downregulating the expressions of CXCR-4, ICAM-1, and VEGF in 4 to 14 days after AMI. Immunohistochemistry analysis showed that rosuvastatin treatment was associated with increased accumulation of CD90+, CD133+, and c-kit+ progenitor cells in the peri-infarction region. Masson staining and echocardiograph confirmed that rosuvastatin could attenuate left ventricular remodeling and improve postinfarction systolic function.
Conclusion:
The data suggest that rosuvastatin can protect the heart from ischemic injury and preserve the cardiac function in rats in vivo. The changing expressions of SDF-1, CXCR-4, ICAM-1, and VEGF, and the accumulation of progenitor cells were involved in this process.
