Zhou Hao, Ren Yan, Xiao Jun, He Jian, Zhang Yuling, Qiu Zhihuang, Huang Qiuyu, Hu Yunnan, Chen Liangwan
Department of Cardiac Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Key Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
Ann Transl Med. 2021 Oct;9(20):1574. doi: 10.21037/atm-21-4933.
The precise role collagen plays in acute aortic dissection (AAD) was investigated in an animal model of β-aminopropinitrile (BAPN)-induced AAD.
The 30 3-week-old male specific-pathogen free (SPF)-grade Sprague-Dawley (SD) rats were randomly divided into two groups: 10 in the Control group and 20 in the Model group. The Model group was treated with 0.1% BAPN for 4 weeks, while the Control group received untreated water. Histopathological staining and western blot were used to detect changes of the extracellular matrix (ECM) and collagen content in the aorta.
At the end of the experiment, the incidence of AAD was 25%, the aortic ECM of surviving rats was severely damaged, and the arrangement was disordered. Fibroblast cells are unevenly distributed, with wide gaps, collagen fibers were also distributed unevenly in a disordered arrangement and their thickness was uneven. The elastic membrane disappeared over a large area. Compare to Control group, the Collagen types I, III and their subunits were upregulated (P<0.05), while matrix metalloproteinase (MMP) 2 and MMP9 were downregulated in the aorta of Model group (P<0.05).
In the animal model of BAPN-induced AAD, collagen types I, III and subunits were increased, while MMP2 and MMP9 were decreased in thoracic aorta, which may lead to stiffness of the aorta and be the cause of dissection.
在β-氨基丙腈（BAPN）诱导的急性主动脉夹层（AAD）动物模型中研究了胶原蛋白在AAD中的确切作用。
将30只3周龄雄性无特定病原体（SPF）级别的Sprague-Dawley（SD）大鼠随机分为两组：对照组10只，模型组20只。模型组用0.1% BAPN处理4周，而对照组给予未处理的水。采用组织病理学染色和蛋白质印迹法检测主动脉中细胞外基质（ECM）和胶原蛋白含量的变化。
实验结束时，AAD的发生率为25%，存活大鼠的主动脉ECM严重受损，排列紊乱。成纤维细胞分布不均，间隙宽大，胶原纤维也分布不均，排列紊乱，厚度不均。弹性膜大面积消失。与对照组相比，模型组主动脉中I型、III型胶原蛋白及其亚基上调（P<0.05），而基质金属蛋白酶（MMP）2和MMP9下调（P<0.05）。
在BAPN诱导的AAD动物模型中，胸主动脉中I型、III型胶原蛋白及其亚基增加，而MMP2和MMP9减少，这可能导致主动脉僵硬并成为夹层的原因。
