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DBA/2小鼠左心室功能障碍合并CAWS动脉炎的模型

A Model of Left Ventricular Dysfunction Complicated by CAWS Arteritis in DBA/2 Mice.

作者信息

Hirata Naoto, Ishibashi Ken-Ichi, Usui Tatsuya, Yoshioka Jiro, Hata Satoru, Adachi Yoshiyuki, Nagi-Miura Noriko, Ohta Shin, Ohno Naohito

机构信息

Department of Pharmacy, Nagano Red Cross Hospital, 5-22-1 Wakasato, Nagano, Nagano 380-8582, Japan.

出版信息

Int J Vasc Med. 2012;2012:570297. doi: 10.1155/2012/570297. Epub 2012 Jul 8.

DOI:10.1155/2012/570297
PMID:22830029
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3399367/
Abstract

It was reported previously that a Candida albicans water-soluble fraction (CAWS), including a mannoprotein and β-glucan complex, has strong potency in inducing fatal necrotizing arteritis in DBA/2 mice. In this study, histopathological changes and cardiac function were investigated in this system. One mg/day of CAWS was given to DBA/2 mice via peritoneal injection for five days. The CAWS-treated DBA/2 mice were induced aortitis and died at an incidence of 100% within several weeks. Histological findings included stenosis in the left ventricular outflow tract (LVOT) and severe inflammatory changes of the aortic valve with fibrinoid necrosis. Cardiomegaly was observed and heart weight increased 1.62 fold (P < 0.01). Echocardiography revealed a severe reduction in contractility and dilatation of the cavity in the left ventricle (LV): LV fractional shortening (LVFS) decreased from 71% to 38% (P < 0.01), and the LV end-diastolic diameter (LVDd) increased from 2.21 mm to 3.26 mm (P < 0.01). The titer of BNP mRNA increased in the CAWS-treated group. Severe inflammatory changes resulting from CAWS brought about lethal LV dysfunction by aortic valve deformation with LVOT stenosis. This system is proposed as an easy and useful experimental model of heart failure because CAWS arteritis can be induced by CAWS injection alone.

摘要

先前有报道称,白色念珠菌水溶性组分(CAWS),包括甘露糖蛋白和β-葡聚糖复合物,在诱导DBA/2小鼠发生致命性坏死性动脉炎方面具有很强的效力。在本研究中,对该系统中的组织病理学变化和心脏功能进行了研究。通过腹腔注射,每天给DBA/2小鼠注射1 mg CAWS,持续五天。经CAWS处理的DBA/2小鼠发生主动脉炎,并在几周内100%死亡。组织学检查结果包括左心室流出道(LVOT)狭窄以及主动脉瓣严重炎症改变伴纤维蛋白样坏死。观察到心脏肥大,心脏重量增加了1.62倍(P < 0.01)。超声心动图显示左心室(LV)收缩力严重降低且腔室扩张:左心室短轴缩短率(LVFS)从71%降至38%(P < 0.01),左心室舒张末期直径(LVDd)从2.21 mm增加到3.26 mm(P < 0.01)。CAWS处理组中BNP mRNA的滴度增加。CAWS引起的严重炎症变化通过伴有LVOT狭窄的主动脉瓣变形导致致命的左心室功能障碍。由于仅通过注射CAWS即可诱导CAWS动脉炎,因此该系统被提议作为一种简单且有用的心力衰竭实验模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/287106b149e8/IJVM2012-570297.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/8664f7f21a4c/IJVM2012-570297.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/0daee9c4181b/IJVM2012-570297.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/be555d5ffda0/IJVM2012-570297.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/23ec0d3b1f0f/IJVM2012-570297.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/0c08d8cbf09b/IJVM2012-570297.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/ab25a52ff2e8/IJVM2012-570297.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/59bf00af95ad/IJVM2012-570297.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/287106b149e8/IJVM2012-570297.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/8664f7f21a4c/IJVM2012-570297.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/0daee9c4181b/IJVM2012-570297.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/be555d5ffda0/IJVM2012-570297.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/23ec0d3b1f0f/IJVM2012-570297.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/0c08d8cbf09b/IJVM2012-570297.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/ab25a52ff2e8/IJVM2012-570297.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/59bf00af95ad/IJVM2012-570297.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca17/3399367/287106b149e8/IJVM2012-570297.008.jpg

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