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利用同步辐射检测延迟水母螫伤综合征小鼠的微血管改变。

Detection of microvasculature alterations by synchrotron radiation in murine with delayed jellyfish envenomation syndrome.

机构信息

Department of Marine Biotechnology, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, China.

Northern Hospital, General Hospital of PLA Shenyang Military Area Command, Shenyang 110031, China.

出版信息

Toxicon. 2014 Apr;81:48-53. doi: 10.1016/j.toxicon.2014.01.017. Epub 2014 Feb 6.

DOI:10.1016/j.toxicon.2014.01.017
PMID:24508769
Abstract

Using the tentacle extract (TE) from the jellyfish Cyanea capillata, we have previously established a delayed jellyfish envenomation syndrome (DJES) model, which is meaningful for clinical interventions against jellyfish stings. However, the mechanism of DJES still remains unclear. Thus, this study aimed to explore its potential mechanism by detecting TE-induced microvasculature alterations in vivo and ex vivo. Using a third-generation synchrotron radiation facility, we, for the first time, directly observed the blood vessel alterations induced by jellyfish venom in vivo and ex vivo. Firstly, microvasculature imaging of whole-body mouse in vivo indicated that the small blood vessel branches in the liver and kidney in the TE-treated group, seemed much thinner than those in the control group. Secondly, 3D imaging of kidney ex vivo showed that the kidneys in the TE-treated group had incomplete vascular trees where distal vessel branches were partly missing and disorderly disturbed. Finally, histopathological analysis found that obvious morphological changes, especially hemorrhagic effects, were also present in the TE-treated kidney. Thus, TE-induced microvasculature changes might be one of the important mechanisms of multiple organ dysfunctions in DJES. In addition, the methods we employed here will probably facilitate further studies on developing effective intervention strategies against DJES.

摘要

我们曾利用海蜇 Cyanea capillata 的触手提取物 (TE) 建立了延迟海蜇蜇伤综合征 (DJES) 模型,这对于临床干预海蜇蜇伤具有重要意义。然而,DJES 的发病机制仍不清楚。因此,本研究旨在通过检测体内和体外 TE 诱导的微血管改变来探讨其潜在机制。本研究首次利用第三代同步辐射装置,直接观察到了海蜇毒液在体内和体外诱导的血管改变。首先,对整体小鼠的微血管成像显示,TE 处理组的肝、肾中小血管分支比对照组的血管分支明显更细。其次,对离体肾脏的 3D 成像显示,TE 处理组的肾脏血管树不完整,远端血管分支部分缺失,排列紊乱。最后,组织病理学分析发现,TE 处理的肾脏也存在明显的形态学改变,特别是出血效应。因此,TE 诱导的微血管改变可能是 DJES 多器官功能障碍的重要机制之一。此外,我们所采用的方法可能有助于进一步研究开发针对 DJES 的有效干预策略。

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