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甘草素通过抑制纤维化和炎症减轻高果糖喂养诱导的心脏损伤。

Liquiritigenin attenuates cardiac injury induced by high fructose-feeding through fibrosis and inflammation suppression.

机构信息

Department of Cardiology, Huai'an First Affiliated Hospital, Nanjing Medical University, Huai'an 223300, China.

出版信息

Biomed Pharmacother. 2017 Feb;86:694-704. doi: 10.1016/j.biopha.2016.12.066. Epub 2016 Dec 28.

DOI:10.1016/j.biopha.2016.12.066
PMID:28039849
Abstract

Diabetes combined with cardiomyopathy is considered as an essential complication, showing diastolic persistently and causing cardiac injury, which is linked to fibrosis progression and inflammation response. Fibrosis and inflammation response are two markers for cardiomyopathy. Liquiritigenin is a flavanone, isolated from Radix glycyrrhiza, which exhibits various biological properties, including anti-cancer and anti-inflammatory activities. Here, in our study, the protective effects and anti-inflammatory activity of liquiritigenin were explored in mice and cardiac muscle cells treated by fructose to reveal the possible mechanism by which liquiritigenin attenuates cardiac injury. The mice were separated into five groups. The diabetic model of mouse was established with 30% high fructose feeding. Liquiritigenin dramatically reduced the lipid accumulation induced by high fructose diet. Compared to mice only treated with high fructose, mice in the presence of liquiritigenin after fructose feeding developed less cardiac fibrosis with lower levels of alpha smooth muscle-actin (α-SMA), Collagen type I, Collagen type II, TGF-β1 and Procol1a1. Additionally, liquiritigenin markedly down-regulated inflammatory cytokines secretion and phosphorylated NF-κB via inhibiting IKKα/IκBα signaling pathway. Our results indicate that liquiritigenin has a protective role in high fructose feeding-triggered cardiac injury through fibrosis and inflammation response suppression by inactivating NF-κB signaling pathway. Thus, liquiritigenin may be a potential candidate for diabetes-associated cardiac injury.

摘要

糖尿病合并心肌病被认为是一种重要的并发症,表现为舒张持续存在,导致心脏损伤,与纤维化进展和炎症反应有关。纤维化和炎症反应是心肌病的两个标志物。甘草素是从甘草根中分离出来的一种黄烷酮,具有多种生物特性,包括抗癌和抗炎活性。在这里,我们在果糖处理的小鼠和心肌细胞中研究了甘草素的保护作用和抗炎活性,以揭示甘草素减轻心脏损伤的可能机制。将小鼠分为五组。用 30%高果糖喂养建立小鼠糖尿病模型。甘草素显著减少了高脂肪果糖饮食引起的脂质积累。与仅用高果糖处理的小鼠相比,果糖喂养后存在甘草素的小鼠心脏纤维化程度降低,α-平滑肌肌动蛋白(α-SMA)、I 型胶原、II 型胶原、TGF-β1 和 Procol1a1 水平降低。此外,甘草素通过抑制 IKKα/IκBα 信号通路显著下调炎症细胞因子的分泌和磷酸化 NF-κB。我们的结果表明,甘草素通过抑制 NF-κB 信号通路抑制纤维化和炎症反应,在高果糖喂养引起的心脏损伤中发挥保护作用。因此,甘草素可能是糖尿病相关心脏损伤的潜在候选药物。

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