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.

Highlights

  • Myocardial hypertrophy (MH), an adaptive response to myocardial overload, is one of the independent risk factors for various cardiovascular diseases [1]

  • Studies have shown that a large number of inflammatory factors participate in the formation of MH [5], including tumor necrosis factor (TNF-ɑ) and interleukin 6 (IL-6) and BioMed Research International other anti-inflammatory factors such as interleukin 10 (IL-10) [6]

  • There was a significant decrease in left ventricular mass index (LVMI) of the MH+aspirin group than that of the MH model group (P < 0:05)

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Summary

Introduction

Myocardial hypertrophy (MH), an adaptive response to myocardial overload, is one of the independent risk factors for various cardiovascular diseases [1]. It is characterized by the proliferation of myocardial connective tissue and the increase of cell volume. Studies have shown that a large number of inflammatory factors participate in the formation of MH (including ventricular remodeling, fibrosis, and apoptosis) [5], including tumor necrosis factor (TNF-ɑ) and interleukin 6 (IL-6) and BioMed Research International other anti-inflammatory factors such as interleukin 10 (IL-10) [6]. Proinflammatory and anti-inflammatory factors can both promote each other and antagonize each other. They maintain a balance to maintain the body’s homeostasis [8]

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