Department of Biochemistry and Molecular Biology, Hengyang Medical School, Hengyang, Hunan 421001, P.R. China.
Department of Pain, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, P.R. China.
Mol Med Rep. 2022 Jun;25(6). doi: 10.3892/mmr.2022.12730. Epub 2022 May 11.
Endothelial cell (EC) dysfunction is one of the initiating factors of atherosclerosis. EC dysfunction is primarily caused by oxidative damage and inflammation. As a classic non‑specific antioxidant and anti‑inflammatory drug, curcumin has been widely used in studies of lipid metabolism disorders. However, whether curcumin is able to alleviate HO‑induced EC damage and its related mechanisms has remained to be elucidated. The present study confirmed the protective effects of curcumin on human umbilical vein endothelial cells (HUVECs). A HUVEC injury model was established using HO and the optimal concentrations and time of curcumin to achieve therapeutic effects were explored. Curcumin was observed to inhibit HO‑induced pyroptosis by inhibiting the activation of NOD‑, LRR‑ and pyrin domain‑containing protein 3. In addition, curcumin improved HUVEC function by restoring αvβ3 and reducing endothelin‑1 expression. In conclusion, the results of the present study revealed the mechanism through which curcumin inhibits pyroptosis and indicated that curcumin may have a potential utility in treating diseases of EC dysfunction.
内皮细胞 (EC) 功能障碍是动脉粥样硬化的起始因素之一。EC 功能障碍主要由氧化损伤和炎症引起。姜黄素作为一种经典的非特异性抗氧化剂和抗炎药物,已广泛应用于脂质代谢紊乱的研究中。然而,姜黄素是否能够减轻 HO 诱导的 EC 损伤及其相关机制仍有待阐明。本研究证实了姜黄素对人脐静脉内皮细胞 (HUVEC) 的保护作用。使用 HO 建立 HUVEC 损伤模型,探讨了姜黄素达到治疗效果的最佳浓度和时间。结果表明,姜黄素通过抑制 NOD、LRR 和 pyrin 结构域蛋白 3 的激活,抑制 HO 诱导的细胞焦亡。此外,姜黄素通过恢复 αvβ3 和减少内皮素-1 的表达来改善 HUVEC 功能。综上所述,本研究揭示了姜黄素抑制细胞焦亡的机制,并表明姜黄素在治疗 EC 功能障碍相关疾病方面可能具有潜在的应用价值。