Department of Cardiothoracic Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Department of Cardiology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.
Cardiovasc Pathol. 2017 Nov-Dec;31:57-62. doi: 10.1016/j.carpath.2017.08.001. Epub 2017 Aug 10.
Oxidized low-density lipoprotein (ox-LDL) has been reported to induce apoptosis of endothelial cells (ECs) and contribute to the progression of atherosclerosis. Kaempferol has been shown to possess antiatherosclerotic effect. The aim of the present study was to evaluate the effect of kaempferol on ox-LDL-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and its possible molecular basis. The results showed that kaempferol alleviated ox-LDL-induced apoptosis. Kaempferol increased the ratio of LC3-II/I and beclin-1 level in ox-LDL-induced HUVECs. Moreover, the expression of p-Akt and p-mTOR was down-regulated after treatment with kaempferol in ox-LDL-treated HUVECs, which is similar to the effect of PI3K inhibitor (LY294002) or mTOR inhibitor [rapamycin (RAP)]. Besides, autophagy induced by kaempferol was enhanced by LY294002 or RAP, while kaempferol-induced autophagy was attenuated with insulin treatment, the activator of PI3K/Akt/mTOR pathway. Furthermore, insulin also abated the effect of kaempferol on cell viability and apoptosis in ox-LDL-induced HUVECs. The results indicated that kaempferol alleviated ox-LDL-induced cell apoptosis by up-regulation of autophagy via inhibiting PI3K/Akt/mTOR pathway in human ECs.
氧化型低密度脂蛋白（ox-LDL）已被报道可诱导内皮细胞（ECs）凋亡，并促进动脉粥样硬化的进展。山奈酚已被证明具有抗动脉粥样硬化作用。本研究旨在评估山奈酚对 ox-LDL 诱导的人脐静脉内皮细胞（HUVECs）凋亡的影响及其可能的分子基础。结果表明，山奈酚减轻了 ox-LDL 诱导的细胞凋亡。山奈酚增加了 ox-LDL 诱导的 HUVECs 中 LC3-II/I 比值和 beclin-1 水平。此外，在 ox-LDL 处理的 HUVECs 中用山奈酚处理后，p-Akt 和 p-mTOR 的表达下调，这与 PI3K 抑制剂（LY294002）或 mTOR 抑制剂[雷帕霉素（RAP）]的作用相似。此外，LY294002 或 RAP 增强了山奈酚诱导的自噬，而胰岛素处理（PI3K/Akt/mTOR 通路的激活剂）则减弱了山奈酚诱导的自噬。此外，胰岛素也减弱了山奈酚对 ox-LDL 诱导的 HUVECs 中细胞活力和凋亡的作用。结果表明，山奈酚通过抑制 PI3K/Akt/mTOR 通路上调自噬来减轻 ox-LDL 诱导的细胞凋亡。
