Curcumin-mediated Photodynamic Therapy Inhibits the Phenotypic Transformation, Migration, and Foaming of Oxidized Low-density Lipoprotein-treated Vascular Smooth Muscle Cells by Promoting Autophagy.
Curcumin-mediated Photodynamic Therapy Inhibits the Phenotypic Transformation, Migration, and Foaming of Oxidized Low-density Lipoprotein-treated Vascular Smooth Muscle Cells by Promoting Autophagy.
复制标题
姜黄素介导的光动力疗法通过促进自噬抑制氧化低密度脂蛋白处理的血管平滑肌细胞的表型转化、迁移和泡沫
DOI：
10.1097/fjc.0000000000001069
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发表时间：
2021-06-02
影响因子：
3
通讯作者：
Bai D
中科院分区：
文献类型：
--
作者：
Wang G;Zhu Y;Li K;Liao B;Wang F;Shao L;Huang L;Bai D
补充数字内容在文本中可用。血管平滑肌细胞（VSMC）正成为动脉粥样硬化研究的热点和靶点。本研究旨在观察姜黄素（CUR）介导的光动力疗法（CUR-PDT）对氧化低密度脂蛋白（ox-LDL）处理的VSMCs的特异性作用，并证实这些作用是否通过自噬介导。在这项研究中，小鼠主动脉平滑肌细胞系和A7 r5细胞系用于平行实验。通过Cell Counting Kit-8测定法评价VSMC活力。用氧化型低密度脂蛋白（ox-LDL）处理血管平滑肌细胞，建立体外动脉粥样硬化模型。Western blotting检测细胞自噬水平及表型转化相关蛋白的表达。transwell法检测细胞迁移能力。油红O染色检测细胞内脂滴的存在。结果表明，ox-LDL刺激VSMCs后，VSMCs由收缩表型向合成表型转化，自噬被抑制。而CUR-PDT可显著促进ox-LDL诱导的自噬水平，抑制ox-LDL诱导的表型转化过程。此外，ox-LDL显着促进VSMC迁移和增加脂滴的数量，而CUR-PDT治疗显着降低ox-LDL诱导的VSMC迁移能力和脂滴数量的增加。用自噬抑制剂3-methyladenine预处理VSMCs 24 h后，CUR-PDT的作用被逆转。因此，我们的研究表明，CUR-PDT可以抑制ox-LDL处理的VSMCs的表型转化，迁移和泡沫诱导自噬。
Supplemental Digital Content is Available in the Text. Vascular smooth muscle cells (VSMCs) are becoming a hot spot and target of atherosclerosis research. This study aimed to observe the specific effects of curcumin (CUR)-mediated photodynamic therapy (CUR-PDT) on oxidized low-density lipoprotein (ox-LDL)-treated VSMCs and confirm whether these effects are mediated by autophagy. In this study, the mouse aortic smooth muscle cell line and A7r5 cell lines were used for parallel experiments. VSMC viability was evaluated by Cell Counting Kit-8 assay. VSMCs were treated with ox-LDL to establish a model of atherosclerosis in vitro. The autophagy level and the expression of proteins related to phenotypic transformation were detected by western blotting. The migration ability of the cells was detected by using transwell assay. The presence of intracellular lipid droplets was detected by Oil Red O staining. The results showed that VSMCs transformed from the contraction phenotype to the synthetic phenotype when stimulated by ox-LDL, during which autophagy was inhibited. However, CUR-PDT treatment significantly promoted the level of autophagy and inhibited the process of phenotypic transformation induced by ox-LDL. In addition, ox-LDL significantly promoted VSMC migration and increased the number of lipid droplets, whereas CUR-PDT treatment significantly reduced the ox-LDL-induced increase in the migration ability of, and lipid droplet numbers in, VSMCs. When the VSMCs were pretreated with the autophagy inhibitor 3-methyladenine for 24 hours, the effects of CUR-PDT were reversed. Therefore, our study indicated that CUR-PDT can inhibit the phenotypic transformation, migration, and foaming of ox-LDL–treated VSMCs by inducing autophagy.