Periplocymarin protects against myocardial fibrosis induced by β-adrenergic activation in mice.

Periplocymarin protects against myocardial fibrosis induced by β-adrenergic activation in mice.
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Periplocymarin 可以防止小鼠β-肾上腺素能激活引起的心肌纤维化。

DOI:
10.1016/j.biopha.2021.111562
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发表时间:
2021-04
影响因子:
7.5
通讯作者:
Hu Xu
Hu Xu
中科院分区:
医学2区
文献类型:
--
作者:
Weijing Yun;Lei Qian;Ruqiang Yuan;Hu Xu

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杠柳素是杠柳属植物杠柳皮的有效成分,是一种被广泛应用的中药有效成分。本课题组曾报道杠柳素通过促进钙内流而发挥强心作用。然而,其在心肌纤维化发病机制中的确切作用尚未阐明。本研究旨在确定杠柳素在异丙肾上腺素(ISO)诱导的心肌纤维化中的潜在作用及其机制。C57 BL/6小鼠皮下注射ISO(5 mg/kg/天)或盐水1周。通过超声心动图测量的早期心房波比率(E/A比率)显示,给药杠柳香豆素(5 mg/kg/d)可显著逆转ISO诱导的心脏僵硬。Masson三色染色显示杠柳素处理减少了细胞外基质(ECM)的过度沉积。实时荧光定量PCR和蛋白质印迹法进一步证实杠柳香豆素可抑制ISO诱导的肝纤维化相关基因(Col 1a 1、Col 3a 1、Acta 2和Tgfb 1)和蛋白质(Ⅰ型胶原、Ⅲ型胶原、α-SMA和TGF-β1)的表达。代谢组学分析表明杠柳素改善了ISO引起的代谢紊乱,其中许多差异代谢物质参与了氨基酸、葡萄糖和脂质代谢。进一步的网络药理学分析表明,三个关键基因NOS 2、NOS 3和Ptgs 2可能是杠柳毒素的潜在作用靶点。ISO处理后,心肌组织NOS 3 mRNA表达降低,Ptgs 2 mRNA表达增加,杠柳香豆素可逆转上述变化。Ptgs 2编码蛋白考克斯-2的表达与Ptgs 2 mRNA的表达一致,而eNOS的表达无明显变化。体外研究表明杠柳素至少通过调节心肌细胞eNOS和考克斯-2发挥抗纤维化作用。杠柳苷对β-肾上腺素能激活诱导的心肌纤维化具有保护作用,其机制可能是通过至少靶向eNOS和考克斯-2,改善心肌细胞代谢过程,从而减轻心肌纤维化。我们的研究表明杠柳素是一种潜在的预防心肌纤维化的治疗药物。
Periplocymarin is an effective component of Periplocae Cortex, which was wildly used as an ingredient in Traditional Chinese Medicine. Our group previously reported that periplocymarin exerted cardiotonic role via promoting calcium influx. However, its exact role in the pathogenesis of myocardial fibrosis has not been elucidated yet. The present study was aimed at determining the potential effect and underlying mechanism of periplocymarin in isoproterenol (ISO)-induced myocardial fibrosis. C57BL/6 mice were subcutaneously injected with ISO (5 mg/kg/day) or saline for 1 week. The early-to-atrial wave ratio (E/A ratio) measured by echocardiography revealed that ISO-induced heart stiffness was remarkably reversed by administration of periplocymarin (5 mg/kg/day). Masson trichrome staining exhibited that treatment of periplocymarin reduced the excessive deposition of extracellular matrix (ECM). Further investigations employing real-time PCR and western blot demonstrated that periplocymarin suppressed the expression of fibrosis related genes (Col1a1,Col3a1,Acta2andTgfb1) and proteins (Collagen I, Collagen III, α-SMA and TGF-β1) induced by ISO. Metabolomics analysis demonstrated that periplocymarin ameliorated the disorders triggered by ISO and many of the differential metabolic substances were involved in amino acid, glucose and lipid metabolism. Further analysis using network pharmacology revealed that three key genes, namelyNOS2,NOS3andPtgs2, may be the potential targets of periplocymarin and responsible for the disorders. Validation using heart tissues showed that the mRNA expression ofNOS3was decreased whilePtgs2was increased upon ISO treatment, which were reversed by periplocymarin. Moreover, the expression of COX-2 (Ptgs2encoded protein) was consistent with the aspect of Ptgs2 mRNA, while eNOS (NOS3encoded protein) expression was unchanged. In vitro studies exhibited that periplocymarin exerts anti-fibrotic function via regulating at least eNOS and COX-2 in cardiomyocyte. Taken together, periplocymarin protects against myocardial fibrosis induced by β-adrenergic activation, the potential mechanism was that periplocymarin targeted on, at least eNOS and COX-2, to improve the metabolic processes of cardiomyocyte and thus attenuated the myocardial fibrosis. Our study highlighted that periplocymarin is a potential therapeutic agent for the prevention of myocardial fibrosis.
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发表时间: 2016-03
影响因子: 4.6
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