The role of adipokines in the development of atherosclerosis (AS) has received increasing attention in recent years. This study aimed to explore the effects of chemerin on the functions of human endothelial progenitor cells (EPCs) and to investigate its role in lipid accumulation in ApoE-knockout (ApoE−/−) mice. EPCs were cultured and treated with chemerin together with the specific p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580 in a time- and dose-dependent manner. Changes in migration, adhesion, proliferation and the apoptosis rate of EPCs were detected. ApoE−/− mice with high-fat diet-induced AS were treated with chemerin with or without SB 203580. Weights were recorded, lipid indicators were detected, and tissues sections were stained. The data showed that chemerin enhanced the adhesion and migration abilities of EPCs, and reduced the apoptosis ratio and that this effect might be mediated through the p38 MAPK pathway. Additionally, chemerin increased the instability of plaques. Compared with the control group and the inhibitor group, ApoE−/− mice treated with chemerin protein had more serious arterial stenosis, higher lipid contents in plaques and decreased collagen. Lipid accumulation in the liver and kidney and inflammation in the hepatic portal area were enhanced by treatment with chemerin, and the size of adipocytes also increased after chemerin treatment. In conclusion, chemerin can enhance the adhesion and migration abilities of human EPCs and reduce the apoptosis ratio. In animals, chemerin can increase lipid accumulation in atherosclerotic plaques and exacerbate plaques instability. At the same time, chemerin can cause abnormal lipid accumulation in the livers and kidneys of model animals. After specifically blocking the p38 MAPK pathway, the effect of chemerin was reduced. In conclusion, this study showed that chemerin enhances the adhesion and migration abilities of EPCs and increases the instability of plaques and abnormal lipid accumulation in ApoE−/− mice. Furthermore, these effects might be mediated through the p38 MAPK pathway.

中文翻译：

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Chemerin增强人内皮祖细胞的粘附和迁移，并增加动脉粥样硬化小鼠的脂质蓄积。

近年来，脂肪因子在动脉粥样硬化（AS）发展中的作用受到越来越多的关注。这项研究旨在探讨chemerin对人内皮祖细胞（EPC）功能的影响，并研究其在ApoE基因敲除（ApoE-/-）小鼠脂质蓄积中的作用。培养EPC，并用chemerin和特异性p38丝裂原活化蛋白激酶（MAPK）抑制剂SB 203580进行时间和剂量依赖性处理。检测了EPC的迁移，粘附，增殖和凋亡率的变化。高脂饮食诱导的AS的ApoE-/-小鼠用含或不含SB 203580的凯莫瑞处理。记录体重，检测脂质指标，并对组织切片染色。数据显示chemerin增强了EPC的粘附和迁移能力，并降低了细胞凋亡率，并且这种作用可能是通过p38 MAPK途径介导的。另外，凯莫瑞增加了斑块的不稳定性。与chemerin蛋白治疗的ApoE-/-小鼠相比，对照组和抑制剂组的动脉狭窄更严重，斑块中脂质含量更高，胶原蛋白减少。凯莫瑞治疗可增强肝脏和肾脏中脂质的积累和肝门区的炎症，凯莫瑞治疗后脂肪细胞的大小也会增加。总之，凯莫瑞可以增强人EPC的黏附和迁移能力，并降低细胞凋亡率。在动物中，凯莫瑞可以增加动脉粥样硬化斑块中的脂质蓄积，并加剧斑块的不稳定性。同时，凯莫瑞可以引起模型动物肝脏和肾脏中脂质的异常蓄积。在特异性阻断p38 MAPK途径后，凯莫瑞的作用降低。总之，这项研究表明凯莫瑞增强了ApoE-/-小鼠EPC的粘附和迁移能力，并增加了斑块的不稳定性和脂质的异常积累。此外，这些作用可能是通过p38 MAPK途径介导的。