Abstract
Objective. To investigate the effect of beraprost sodium (BPS) on diabetic cardiomyopathy and the underlying mechanism. Methods. A total of 40 Sprague Dawley rats were randomly divided into the normal control group (N = 10) and the model group (N = 30). The model group was fed a high-fat diet followed by a one-time dose of streptozotocin (STZ) to establish the diabetes mellitus model. After that, rats were randomly divided into two groups with or without BPS intervention. After 8 weeks, we explored the role of the p38 MAPK signaling pathway in inflammation, oxidative stress, cardiac morphology, and myocardial apoptosis. Results. Compared with control, the ratio of heart-weight to body-weight and the serum levels of SOD and GSH in the BPS group significantly increased, the expression of p38 MAPK, the serum levels of MDA, TGF-β1, TNF-α, HIF-1α, MMP-9, caspase-3, BNP, ANP, and heart Bax expression significantly decreased, and heart Bcl-2 expression significantly increased. H&E staining in diabetic rats showed the cardiac muscle fibers derangement, the widening gap, the pyknotic and fragmented nuclei, and more apoptosis. Conclusions. BPS effectively showed protective effects on diabetic myocardial cells, possibly through the inhibition of p38 MAPK signaling pathway.
Highlights
Epidemiological studies indicate that more than 70% of diabetes mellitus (DM) patients die of cardiovascular disease (CVD); this number is 2-3 times higher than the mortality of CVD in the nondiabetic population [1]
This study showed that through the inhibition of the p38 Mitogen-activated protein kinases (MAPKs) signaling pathway activity, beraprost sodium (BPS) reduced the expression of inflammatory factors such as Tumor necrosis factor-α hypoxia inducible factor 1α subunit (HIF-1α) (TNF-α), HIF-1α, and matrix metalloproteinase-9 (MMP-9); inhibited myocardial cell apoptosis; and decreased the expression of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP), delaying the progression of Diabetic cardiomyopathy (DCM) and protecting cardiac function
The MAPK family plays an important role in intracellular signal transduction and the onset and development of CVD; in particular, the p38 MAPK signaling pathway is closely associated with the onset and development of DCM [6, 15,16,17,18]. p38 MAPK uses a highly conserved three-kinase cascade to transduce signals
Summary
Epidemiological studies indicate that more than 70% of diabetes mellitus (DM) patients die of cardiovascular disease (CVD); this number is 2-3 times higher than the mortality of CVD in the nondiabetic population [1]. The prevention of cardiovascular events is a very important goal in the treatment of DM. Diabetic cardiomyopathy (DCM) is one of the major cardiac complications in DM patients. The incidence of DCM is very high, and the disease is highly dangerous, directly causing mortality due to cardiovascular events in DM patients. Many large-scale studies confirmed that a reduction in hemoglobin A1C (HbA1C) alone did not benefit the primary cardiovascular endpoint. In addition to the control of blood sugar, studying and developing new types of antidiabetic drugs for cardiovascular protection have become popular in the field of DM research
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