Endothelial cell (EC) dysfunction is a major symptom associated with the initiation of atherosclerosis (AS). Cyanidin‐3‐O‐glucoside (C3G) has the potentials to attenuate AS symptoms. In the current study, the mechanism driving the effects of C3G on AS rabbits and injured ECs were explored by focusing on the changes in miR‐204‐5p/SIRT1 axis. AS symptoms were induced in rabbits using high‐fatty diet (HFD) plus balloon catheter injured method and handled with C3G of two doses. Then the changes in artery wall structure, hemodynamics parameters, blood lipid level, systemic inflammation, and miR‐204‐5p/SIRT1 axis were detected. EC dysfunction was imitated by subjecting human umbilical vein endothelial cells (HUVECs) to TNF‐α, which was then handled with C3G. The changes in apoptosis, inflammation, and miR‐204‐5p/SIRT1 axis were detected. The results showed that the administrations of C3G improved artery wall structure and hemodynamics parameters, decreased blood lipid levels, and suppressed pro‐inflammatory cytokine production in HFD rabbits, which was associated with the down‐regulation of miR‐204‐5p and the up‐regulation of SIRT1. In in vitro assays, the treatments of C3G suppressed apoptosis, inhibited inflammation, down‐regulated miR‐204‐5p level, and induced SIRT1 level in HUVECs. The overexpression of miR‐204‐5p impaired the protective effects of C3G on the injured HUVECs by increasing cell apoptosis and inflammation. The findings outlined in the current study confirmed the protective effects of C3G on EC function, which was associated with the down‐regulation of miR‐204‐5p and the up‐regulation of SIRT1.

中文翻译：

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Cyanidin-3-O-glucoside 通过调节 miR-204-5p/SIRT1 介导的炎症和细胞凋亡来减轻内皮细胞功能障碍。

内皮细胞 (EC) 功能障碍是与动脉粥样硬化 (AS) 发生相关的主要症状。Cyanidin-3- O‐葡萄糖苷 (C3G) 具有减轻 AS 症状的潜力。在目前的研究中，通过关注 miR-204-5p/SIRT1 轴的变化，探索了驱动 C3G 对 AS 兔和受损 ECs 影响的机制。使用高脂肪饮食 (HFD) 加球囊导管损伤方法在兔中诱发 AS 症状，并用两剂 C3G 处理。然后检测动脉壁结构、血流动力学参数、血脂水平、全身炎症和 miR-204-5p/SIRT1 轴的变化。通过将人脐静脉内皮细胞 (HUVEC) 置于 TNF-α 中，然后用 C3G 处理来模拟 EC 功能障碍。检测细胞凋亡、炎症和 miR-204-5p/SIRT1 轴的变化。结果表明，C3G 的给药改善了动脉壁结构和血流动力学参数，降低血脂水平，抑制 HFD 兔促炎细胞因子的产生，这与 miR-204-5p 的下调和 SIRT1 的上调有关。在体外试验中，C3G 的治疗抑制了细胞凋亡、抑制炎症、下调 miR-204-5p 水平并诱导 HUVEC 中的 SIRT1 水平。miR-204-5p的过表达通过增加细胞凋亡和炎症来削弱C3G对受损HUVEC的保护作用。当前研究中概述的发现证实了 C3G 对 EC 功能的保护作用，这与 miR-204-5p 的下调和 SIRT1 的上调有关。在体外试验中，C3G 的治疗抑制了细胞凋亡、抑制炎症、下调 miR-204-5p 水平并诱导 HUVEC 中的 SIRT1 水平。miR-204-5p的过表达通过增加细胞凋亡和炎症来削弱C3G对受损HUVEC的保护作用。当前研究中概述的发现证实了 C3G 对 EC 功能的保护作用，这与 miR-204-5p 的下调和 SIRT1 的上调有关。在体外试验中，C3G 的治疗抑制了细胞凋亡、抑制炎症、下调 miR-204-5p 水平并诱导 HUVEC 中的 SIRT1 水平。miR-204-5p的过表达通过增加细胞凋亡和炎症来削弱C3G对受损HUVEC的保护作用。当前研究中概述的发现证实了 C3G 对 EC 功能的保护作用，这与 miR-204-5p 的下调和 SIRT1 的上调有关。