Corilagin ameliorates atherosclerosis by regulating MMP-1,-2, and-9 expression in vitro and in vivo
Corilagin ameliorates atherosclerosis by regulating MMP-1,-2, and-9 expression in vitro and in vivo
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Corilagin 通过调节体外和体内 MMP-1、-2 和-9 的表达来改善动脉粥样硬化
DOI：
10.1016/j.ejphar.2021.174200
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发表时间：
2021-06-12
影响因子：
5
通讯作者：
Chen, Peng
中科院分区：
文献类型：
--
作者：
Tao, Yiting;Zhang, Li;Chen, Peng
Corilagin 是一种多酚，已被鉴定具有抗炎特性。然而，柯里拉金的抗动脉粥样硬化作用尚不清楚。在这里，我们评估了柯里拉金的抗动脉粥样硬化作用及其潜在机制。我们还在体外和体内验证了柯里拉京是否可以通过调节基质金属蛋白酶（MMP）-1、-2和-9来逆转动脉粥样硬化。采用高脂饲料喂养联合球囊损伤的方法建立小型猪动脉粥样硬化模型，监测不同浓度柯里拉京对小型猪颈总动脉粥样硬化的影响。培养鼠RAW264.7巨噬细胞并用氧化低密度脂蛋白诱导；荧光显微镜显示NF-kappa B的核转位。此外，通过免疫组织化学、蛋白质印迹和RT-PCR检测颈总动脉斑块和细胞模型中MMP-1、-2和-9的表达。病理结果提示，模型对照组血管内膜明显增厚，胶原纤维大量沉积，内皮细胞损伤脱落，动脉壁不同程度出现斑块和泡沫细胞形成，并有脂质沉积。柯里拉金治疗显着减轻了颈总动脉的损伤程度，并减少了脂质斑块和泡沫细胞的数量。此外，corilagin 下调颈总动脉斑块和细胞模型中 MMP-1、-2 和-9 的表达。此外，柯里拉京在体外显着抑制 NF-κ B 核转位。总体而言，柯里拉京通过下调 MMP1、-2 和-9 的表达，对实验性动脉粥样硬化小型猪发挥了显着的治疗作用。
Corilagin is a polyphenol has been identified anti-inflammatory properties. However, the anti-atherosclerotic effects of corilagin are not well understood. Here, we evaluated the anti-atherosclerotic effects and the underlying mechanisms of corilagin. We also verified whether corilagin can reverse atherosclerosis by regulating matrix metalloproteinase (MMP)-1,-2, and-9 in vitro and in vivo. An atherosclerosis model was established by feeding minipigs a high-fat diet combined with balloon injury, and the effects of different concentrations of corilagin on common carotid artery atherosclerosis in minipigs were monitored. Murine RAW264.7 macrophages were cultured and induced with oxidized low-density lipoprotein; fluorescence microscopy revealed the nuclear translocation of NF-kappa B. Furthermore, MMP-1,-2, and-9 expression in common carotid artery plaques and cellular models was detected by immunohistochemistry, western blotting, and RT-PCR. The pathological results suggested that the vascular intima of the model control group was significantly thickened, a large amount of collagen fibers was deposited, endothelial cells were damaged and detached, and plaque and foam cell formation occurred to varying degrees on the arterial wall, with lipid deposition. Corilagin treatment significantly reduced the degree of injury in the common carotid artery and decreased the number of lipid plaques and foam cells. Additionally, corilagin downregulated MMP-1,-2, and-9 expression in the common carotid artery plaques and cellular model. Moreover, corilagin significantly inhibited NF-kappa B nuclear translocation in vitro. Overall, corilagin exerted substantial therapeutic effects on experimental atherosclerotic minipigs via the downregulation of MMP1,-2, and-9 expression.