Honokiol plays an important role in anti-oxidation, but its role in diabetic vascular complications is unclear. In this study, the effects of honokiol in high glucose/high fat (HG/HF)-induced human umbilical vein endothelial cells (HUVECs) were explored. After pre-treatment with honokiol, the cells were transferred to an HG/HF medium, and cell viability and apoptosis were respectively measured by methyl tetrazolium and flow cytometry. Moreover, the contents of reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) were measured. The expressions of C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), phosphorylated-protein kinase RNA-like endoplasmic reticulum kinase (p-PERK), phosphorylated-inositol requiring enzyme-1α (p-IRE1α), cleaved caspase-3 and SIRT1 were determined by Western blot or quantitative reverse transcription PCR, respectively. Finally, the viability, apoptosis, and the contents of ROS, MDA, and SOD, as well as the expressions of CHOP, GRP78, p-PERK, p-IRE1α, cleaved caspase-3, Akt, p-Akt, and SIRT1 in the cells transfected with small interfering RNA SIRT1 (siSIRT1) were detected by the previously mentioned methods. Honokiol reversed the effect of HG/HF on promoting cell apoptosis, ROS and MDA contents, and the expressions of CHOP, GRP78, p-PERK, p-IRE1α and cleaved caspase-3, and also reversed the inhibitory effect of HG/HF on cell viability, SOD content and SIRT1 expression. However, siSIRT1 reversed the above effects caused by honokiol. Honokiol activated SIRT1 promoter. SIRT1 interacted with Akt, consequently promoting the activity of Akt. Therefore, honokiol activates the Akt pathway by regulating SIRT1 expression to regulate endoplasmic reticulum stress, promotes cell viability and inhibits the apoptosis of HG/HF-induced HUVECs.

和厚朴酚在抗氧化中起重要作用，但其在糖尿病血管并发症中的作用尚不清楚。本研究探讨了和厚朴酚在高糖/高脂 (HG/HF) 诱导的人脐静脉内皮细胞 (HUVECs) 中的作用。用和厚朴酚预处理后，将细胞转移到HG/HF培养基中，分别用甲基四唑和流式细胞仪检测细胞活力和凋亡。此外，还测定了活性氧（ROS）、丙二醛（MDA）和超氧化物歧化酶（SOD）的含量。C/EBP 同源蛋白 (CHOP)、葡萄糖调节蛋白 78 (GRP78)、磷酸化蛋白激酶 RNA 样内质网激酶 (p-PERK)、磷酸化肌醇需要酶 1α (p-IRE1α)、分别通过蛋白质印迹或定量逆转录 PCR 测定切割的 caspase-3 和 SIRT1。最后，研究细胞活性、细胞凋亡、ROS、MDA、SOD含量，以及CHOP、GRP78、p-PERK、p-IRE1α、cleaved caspase-3、Akt、p-Akt和SIRT1的表达情况。通过前面提到的方法检测转染了小干扰RNA SIRT1（siSIRT1）的细胞。和厚朴酚逆转 HG/HF 促进细胞凋亡、ROS 和 MDA 含量，以及 CHOP、GRP78、p-PERK、p-IRE1α 和 cleaved caspase-3 的表达，并逆转 HG/HF 对细胞凋亡的抑制作用。细胞活力、SOD 含量和 SIRT1 表达。然而，siSIRT1 逆转了和厚朴引起的上述影响。和厚朴激活的 SIRT1 启动子。SIRT1 与 Akt 相互作用，从而促进 Akt 的活性。所以，