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Fgl2凝血酶原酶在2型糖尿病大鼠心脏微血管内皮细胞中的表达及意义

Expression and significance of fgl2 prothrombinase in cardiac microvascular endothelial cells of rats with type 2 diabetes.

作者信息

Ding Yanping, Liu Kun, Wang Yan, Su Guanhua, Deng Heping, Zeng Qiutang, Liao Yuhua, Wang Zhaohui

机构信息

Department of Cardiology, Huazhong University of Science and Technology, Wuhan, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2010 Oct;30(5):575-81. doi: 10.1007/s11596-010-0545-y. Epub 2010 Nov 10.

Abstract

Microthrombosis may be involved in the pathogenesis of cardiac microangiopathy due to diabetes. Recent studies have shown that fibrinogen-like protein 2 (fgl2) plays a pivotal role in microthrombosis in viral hepatitis, acute vascular xenograft rejection and cytokine-induced fetal loss syndrome. The current study was designed to examine the expression of fgl2 in microvascular endothelial cells and investigate the effects of microthrombi due to fgl2 on cardiac function and structure in rats with type 2 diabetes. Following induction of type 2 diabetes, 24 rats were observed dynamically. Fgl2 expression and related cardiac microthrombosis were examined. Local or circulating TNF-α was measured. Coronary flow (CF) per min was calculated as an index of cardiac microcirculation. Cardiac function and morphology were evaluated. It was found that Fgl2 was highly expressed in cardiac microvascular endothelial cells of rats with type 2 diabetes, which was promoted by local or circulating TNF-α. The Fgl2 expression was associated with cardiac hyaline microthrombosis. In parallel with the fgl2 expression, CF per min, cardiac diastolic or systolic function and cardiac morphology were aggravated to some extent. It was concluded that in rats with type 2 diabetes, microthrombosis due to fgl2 contributes to the impairment of cardiac diastolic or systolic function and morphological changes.

摘要

微血栓形成可能参与糖尿病所致心脏微血管病变的发病机制。近期研究表明,纤维蛋白原样蛋白2(Fgl2)在病毒性肝炎、急性血管异种移植排斥反应及细胞因子诱导的胎儿丢失综合征的微血栓形成中起关键作用。本研究旨在检测Fgl2在微血管内皮细胞中的表达,并探讨Fgl2所致微血栓对2型糖尿病大鼠心脏功能和结构的影响。诱导2型糖尿病后,对24只大鼠进行动态观察。检测Fgl2表达及相关心脏微血栓形成情况。测定局部或循环中的肿瘤坏死因子-α(TNF-α)。计算每分钟冠状动脉血流量(CF)作为心脏微循环指标。评估心脏功能和形态。结果发现,Fgl2在2型糖尿病大鼠心脏微血管内皮细胞中高表达,局部或循环中的TNF-α可促进其表达。Fgl2表达与心脏透明微血栓形成有关。与Fgl2表达平行,每分钟CF、心脏舒张或收缩功能及心脏形态在一定程度上加重。结论为,在2型糖尿病大鼠中,Fgl2所致微血栓形成导致心脏舒张或收缩功能受损及形态改变。

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