Low molecular weight fucoidan alleviates cardiac dysfunction in diabetic Goto-Kakizaki rats by reducing oxidative stress and cardiomyocyte apoptosis.

Low molecular weight fucoidan alleviates cardiac dysfunction in diabetic Goto-Kakizaki rats by reducing oxidative stress and cardiomyocyte apoptosis.
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低分子量岩藻依聚糖通过减少氧化应激和心肌细胞凋亡来减轻糖尿病 Goto-Kakizaki 大鼠的心脏功能障碍。

DOI:
10.1155/2014/420929
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发表时间:
2014
影响因子:
4.3
通讯作者:
Luo D
Luo D
中科院分区:
医学3区
文献类型:
--
作者:
Yu X;Zhang Q;Cui W;Zeng Z;Yang W;Zhang C;Zhao H;Gao W;Wang X;Luo D

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糖尿病性心肌病(DCM)是以心功能不全和心肌细胞凋亡为特征的疾病。氧化应激被认为是DCM发展的主要因素。本研究旨在评价低分子量岩藻聚糖硫酸酯(LMWF)对糖尿病大鼠心功能的保护作用。2型糖尿病goto-kakizaki大鼠未经治疗或用LMWF(50和100 mg/kg/天)治疗3个月。通过超声心动图和离体心脏灌流评价DCM模型的建立及LMWF对心功能的影响。用H-E或天狼星红染色观察心肌结构变化。功能评价表明,LMWF通过增强心肌收缩力和减轻心脏纤维化对DCM具有有益作用。此外,LMWF对糖尿病心肌细胞活性氧的产生和细胞凋亡有明显的抑制作用。低分子量肝素干预后,糖尿病心肌超氧化物歧化酶活性降低,心肌组织超氧化物歧化酶活性明显改善。此外,LMWF强烈抑制糖尿病心脏和高糖处理的心肌细胞中蛋白激酶C β(氧化应激的重要贡献者)的表达增强。结论:LMWF通过改善PKCβ介导的氧化应激和随后的心肌细胞凋亡对DCM具有保护作用。
Diabetic cardiomyopathy (DCM) is characterized by cardiac dysfunction and cardiomyocyte apoptosis. Oxidative stress is suggested to be the major contributor to the development of DCM. This study was intended to evaluate the protective effect of low molecular weight fucoidan (LMWF) against cardiac dysfunction in diabetic rats. Type 2 diabetic goto-kakizaki rats were untreated or treated with LMWF (50 and 100 mg/kg/day) for three months. The establishment of DCM model and the effects of LMWF on cardiac function were evaluated by echocardiography and isolated heart perfusion. Ventricle staining with H-E or Sirius Red was performed to investigate the structural changes in myocardium. Functional evaluation demonstrated that LMWF has a beneficial effect on DCM by enhancing myocardial contractility and mitigating cardiac fibrosis. Additionally, LMWF exerted significant inhibitory effects on the reactive oxygen species production and myocyte apoptosis in diabetic hearts. The depressed activity of superoxide dismutase in diabetic heart was also improved by intervention with LMWF. Moreover, LMWF robustly inhibited the enhanced expression of protein kinase C β, an important contributor to oxidative stress, in diabetic heart and high glucose-treated cardiomyocytes. In conclusion, LMWF possesses a protective effect against DCM through ameliorations of PKCβ-mediated oxidative stress and subsequent cardiomyocyte apoptosis in diabetes.
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