The Protective Effect of Beraprost Sodium on Diabetic Cardiomyopathy through the Inhibition of the p38 MAPK Signaling Pathway in High-Fat-Induced SD Rats.

The Protective Effect of Beraprost Sodium on Diabetic Cardiomyopathy through the Inhibition of the p38 MAPK Signaling Pathway in High-Fat-Induced SD Rats.
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贝前列素钠通过抑制高脂肪诱导的 SD 大鼠的 p38 MAPK 信号通路对糖尿病心肌病的保护作用。

DOI:
10.1155/2014/901437
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发表时间:
2014
影响因子:
2.8
通讯作者:
Shao J
Shao J
中科院分区:
医学4区
文献类型:
--
作者:
Li J;Peng L;Du H;Wang Y;Lu B;Xu Y;Ye X;Shao J

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客观的。探讨贝前列素钠(BPS)对糖尿病心肌病的影响及其机制。方法。 40只SD大鼠随机分为正常对照组(N=10)和模型组(N=30)。模型组给予高脂饮食后一次性给予链脲佐菌素(STZ)建立糖尿病模型。之后,将大鼠随机分为两组,有或没有BPS干预。 8周后,我们探讨了p38 MAPK信号通路在炎症、氧化应激、心脏形态和心肌细胞凋亡中的作用。结果。与对照组相比,BPS组心脏体重与体重的比值以及血清SOD、GSH含量显着升高,p38 MAPK表达量、血清MDA、TGF-β1、TNF-α、HIF-1α、MMP-9、caspase-3、BNP、ANP、心脏Bax表达量显着降低,心脏Bcl-2表达量显着升高。糖尿病大鼠的H&E染色显示心肌纤维紊乱、间隙扩大、细胞核固缩、破碎、细胞凋亡增多。结论。 BPS对糖尿病心肌细胞具有有效的保护作用,其机制可能是通过抑制p38 MAPK信号通路。
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.
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