ADAMTS13抑制动脉粥样硬化模型小鼠血管炎症  

ADAMTS13 inhibits vascular inflammation in a mouse model of atherosclerosis

作　　者：王萌 赵艺鸿 金圣宇[1] WANG Meng;ZHAO Yi-Hong;JIN Sheng-Yu(Department of Hematology,Affiliated Hospital of Yanbian University,Yanji 133000,Jilin,China)

机构地区：[1]延边大学附属医院血液内科,吉林延吉133000

出　　处：《中国老年学杂志》2024年第16期3933-3937,共5页Chinese Journal of Gerontology

基　　金：国家自然科学基金(81660026,82060032);吉林省教育厅“十三五”科学技术研究项目(吉教科合字〔2016〕273);吉林省自然科学基金面上项目(YDZJ202201ZYTS222)。

摘　　要：目的观察血管性血友病因子(vWF)裂解酶(ADAMTS13)在动脉粥样硬化慢性炎症环境中的作用。方法载脂蛋白E缺乏(ApoE^(-/-))和ADAMTS13^(-/-)ApoE^(-/-)小鼠用高脂肪的西方饮食喂养12 w。心脏冰冻切片采用苏木素-伊红染色,主动脉根部动脉粥样硬化病变进行组织学检查。ApoE^(-/-)和ADAMTS13^(-/-)ApoE^(-/-)小鼠主动脉组织切片免疫组织化学染色后观察巨噬细胞浸润数量。利用活体镜检法观察提睾肌静脉氧化损伤、白细胞移动和黏附。结果ADAMTS13^(-/-)ApoE^(-/-)小鼠主动脉表面及主动脉根部的动脉粥样硬化程度较ApoE^(-/-)小鼠明显严重,ADAMTS13^(-/-)ApoE^(-/-)小鼠主动脉根部动脉粥样硬化斑块形成的范围增加约6.1倍(P<0.05)。与ApoE^(-/-)小鼠比较,ADAMTS13^(-/-)ApoE^(-/-)小鼠白细胞移动速度显著减慢(P<0.001),白细胞滚动数量显著增加(P<0.01),同时伴有巨噬细胞浸润。结论ADAMTS13基因缺陷的动脉粥样硬化小鼠模型在实验中血管炎症反应更加明显,ADAMTS13在动脉粥样硬化的慢性炎症环境中对血管炎症有抑制作用。Objective To observe the role of von Willebrand factor(vWF)lyase(ADAMTS13)in the chronic inflammatory environment of atherosclerosis.Methods Apolipoprotein E-null(ApoE^(-/-))and ADAMTS13^(-/-)ApoE^(-/-)mice were fed with a high-fat western diet for 12 w.The frozen heart was sectioned and stained with hematoxylin-eosin,the atherosclerotic lesions of the aortic root were examined histologically.Numbers of macrophage were observed by immunohistochemical staining of aorta sections in both ApoE^(-/-)and ADAMTS13^(-/-)ApoE^(-/-)mice.Leukocyte rolling and adhesion onto cremaster venules after oxidative injury were determined by in-travital microscopy.Results The degree of atherosclerosis on the aortic surface and root of ADAMTS13^(-/-)ApoE^(-/-)mice was signifi-cantly more serious than that of ApoE^(-/-)mice,and the range of atherosclerotic plaque formation in the aortic root of ADAMTS13^(-/-)ApoE^(-/-)mice was increased by 6.1 times(P<0.05).Compared with ApoE^(-/-)mice,the leukocyte rolling velocity of ADAMTS13^(-/-)ApoE^(-/-)mice was significantly decreased(P<0.001),the number of leukocyte rolling was significantly increased(P<0.01),which was accompanied by macrophage infiltration.Conclusions For the mouse model of atherosclerosis with ADAMTS13 gene defect,the vascular inflammatory reaction is more obvious in the experiment.ADAMTS13 could inhibit the vascular inflammatory response in the chronic inflammatory environment of atherosclerosis.

关 键 词：血管性血友病因子裂解酶 炎症反应 动脉粥样硬化 动物模型 

分 类 号：R543.5[医药卫生—心血管疾病]