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The Protective Effect of Aspirin against Myocardial Hypertrophy in Rats
Xiaolong Wu1,2, Minghui Wei1, Haifeng Zhang3
1Department of Physiology, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010110, China.
Abstract:
The protective effect of aspirin against myocardial hypertrophy (MH) was studied. Model rats of pressure overload MH were prepared by abdominal aortic coarctation. Rats were randomly divided into the sham group (n = 9), MH model group (n = 9), and MH+aspirin group (n = 9), which was, respectively, divided into the 4-week group and 8-week group according to the time of intragastric administration. Arterial blood pressure and left ventricular mass index (LVMI) were measured. Changes in myocardial tissue structure were observed by HE staining, Masson staining, and reticular fiber staining. Cardiomyocyte apoptosis was detected by TUNEL assay. The levels of TNF-α, IL-10, TXA2, and PGI2 in myocardium and plasma were detected by ELISA. The arterial blood pressure in the MH model group was significantly higher than that in the 4- and 8-week sham groups, but that in the MH+aspirin group was significantly lower than that in the MH model group. At 4 and 8 weeks, the LVWI in the MH model group was significantly higher than that in the sham group, but it was significantly reduced after aspirin treatment. The myocardial cell hypertrophy was obvious, collagen fibers were proliferated, and reticular fibers were reduced in the 4- and 8-week MH model groups. Compared with the MH model groups, myocardial cells in the MH+aspirin groups were significantly reduced, the collagen fiber content was significantly reduced, and the reticular fiber content was increased. The apoptotic cardiomyocytes in the 4- and 8-week MH model groups were obviously increased. The apoptosis of myocardial cells in the MH+aspirin groups was obviously decreased. The TNF-α levels in the myocardial tissue of the 4- and 8-week MH model groups were significantly increased, while those of the MH+aspirin groups were significantly decreased. There was no significant change in the IL-10 level or PGI2 level at 4 weeks. At 8 weeks, the PGI2 level was significantly decreased in the MH model group while significantly increased in the MH+aspirin group. The TXA2 levels were significantly increased in the 4- and 8-week MH model groups and those in the 4- and 8-week MH+aspirin groups were significantly lower. Aspirin has an anti-inflammatory effect, can effectively reduce the expression of inflammatory factors, inhibit myocardial apoptosis, and has a certain protective effect against MH.
Insights
Aspirin treatment significantly reduced blood pressure and left ventricular mass index in rats with myocardial hypertrophy (MH). Aspirin also inhibited inflammation and cardiomyocyte apoptosis, demonstrating a protective effect against MH.
Area of Science:
- Cardiology
- Pharmacology
- Pathology
Background:
- Myocardial hypertrophy (MH) is a condition characterized by the enlargement of heart muscle cells.
- Pressure overload is a common cause of MH, leading to significant cardiovascular changes.
- Understanding the protective mechanisms against MH is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of aspirin against pressure overload-induced myocardial hypertrophy in a rat model.
- To evaluate the impact of aspirin on key indicators of cardiac structure, function, and inflammation.
Main Methods:
- Rats underwent abdominal aortic coarctation to induce MH, with groups receiving either a sham procedure, MH induction, or MH induction plus aspirin.
- Blood pressure and left ventricular mass index (LVMI) were measured.
- Histological analysis (HE, Masson, reticular fiber staining), TUNEL assay for apoptosis, and ELISA for inflammatory markers (TNF-α, IL-10) and prostanoids (TXA2, PGI2) were performed.
Main Results:
- Aspirin treatment significantly reduced elevated arterial blood pressure and LVMI in MH model rats.
- Histological examination showed reduced cardiomyocyte hypertrophy, collagen proliferation, and increased reticular fibers in aspirin-treated rats.
- Aspirin significantly decreased cardiomyocyte apoptosis and levels of TNF-α, while increasing PGI2 and decreasing TXA2 levels at 8 weeks.
Conclusions:
- Aspirin exhibits anti-inflammatory properties by reducing inflammatory factor expression.
- Aspirin effectively inhibits myocardial apoptosis in the context of MH.
- Aspirin demonstrates a significant protective effect against pressure overload-induced myocardial hypertrophy.
