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Danhong injection attenuates cardiac injury induced by ischemic and reperfused neuronal cells through regulating arginine vasopressin expression and secretion

机译:丹红注射液通过调节精氨酸加压素的表达和分泌,减轻缺血性和再灌注神经细胞诱导的心脏损伤

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摘要

Ischemic stroke is associated with cardiac myocyte vulnerability through some unknown mechanisms. Arginine vasopressin (AVP) may exert considerable function in the relationship of brain damage and heart failure. Danhong injection (DHI) can protect both stroke and heart failure patients with good efficacy in clinics. The aim of this study is to investigate the mechanism of DHI in heart and brain co-protection effects to determine whether AVP plays key role in this course. In the present study, we found that both the supernatant from oxygen-glucose deprivation (OGD) and reperfused primary rat neuronal cells (PRNCs) and AVP treatment caused significant reduction in cell viability and mitochondrial activity in primary rat cardiac myocytes (RCMs). Besides, DHI had the same protective effects with conivaptan, a dual vasopressin V-1A and V-2 receptor antagonist, in reducing the RCM damage induced by overdose AVP. DHI significantly decreased the injury of both PRNCs and RCMs. Meanwhile, the AVP level was elevated dramatically in OGD and reperfusion PRNCs, and DHI was able to decrease the AVP expression in the injured PRNCs. Therefore, our present results suggested that OGD and reperfusion PRNCs might induce myocyte injury by elevating the AVP expression in PRNCs. The ability of DHI to reinstate AVP level may be one of the mechanisms of its brain and heart co-protection effects. (C) 2016 Elsevier B.V. All rights reserved.
机译:缺血性中风通过某些未知机制与心肌细胞易损性相关。精氨酸加压素(AVP)可能在脑损伤和心力衰竭的关系中发挥重要作用。丹红注射液(DHI)可在临床上为中风和心力衰竭患者提供良好的保护。这项研究的目的是研究DHI在心脏和大脑的共同保护作用中的机制,以确定AVP在此过程中是否起关键作用。在本研究中,我们发现氧葡萄糖剥夺(OGD)的上清液和再灌注的原代大鼠神经元细胞(PRNCs)和AVP处理均导致原代大鼠心肌细胞(RCMs)的细胞活力和线粒体活性显着降低。此外,DHI在减少过量AVP引起的RCM损伤方面与双重血管加压素V-1A和V-2受体拮抗剂conivaptan具有相同的保护作用。 DHI显着降低了PRNC和RCM的损伤。同时,OGD和再灌注PRNC中AVP的水平显着升高,DHI能够降低受损PRNC中的AVP表达。因此,我们目前的结果表明,OGD和再灌注PRNCs可能通过升高PRNCs中的AVP表达来诱导心肌细胞损伤。 DHI恢复AVP水平的能力可能是其大脑和心脏共同保护作用的机制之一。 (C)2016 Elsevier B.V.保留所有权利。

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