Li Guilin, Xu Yurong, Sheng Xuan, Liu Hua, Guo Jingjing, Wang Jiayue, Zhong Qi, Jiang Huaide, Zheng Chaoran, Tan Mengxia, Rao Shenqiang, Yu Yanling, Gao Yun, Li Guodong, Liang Shangdong, Zhu Gaochun
Department of Physiology, Medical College of Nanchang University, Nanchang, China.
Obstetrics and Gynecology Department of First Affiliated Hospital, Nanchang University, Nanchang, China.
Cell Physiol Biochem. 2017;42(6):2540-2551. doi: 10.1159/000480215. Epub 2017 Aug 23.
BACKGROUND/AIMS: The induction of endothelial injury by hyperglycemia in diabetes has been widely accepted. Naringin is a bio-flavonoid. Some studies showed that naringin alleviates diabetic complications, but the exact mechanisms by which naringin improves diabetic anomalies are not yet fully understood. The aim of this research was to study the protective effect of naringin on high glucose-induced injury of human umbilical vein endothelial cells (HUVECs).
HUVECs were cultured with or without high glucose in the absence or presence of naringin for 5 days. The expression of CX3CL1 was determined by quantitative real-time RT-PCR (qPCR) and western blot. The cellular bioenergetic analysis oxygen consumption rate (OCR) was measured with a Seahorse Bioscience XF analyzer.
The production of reactive oxygen species (ROS), the expression of CX3CL1 and the level of AKT phosphorylation were increased in HUVECs cultured with high glucose compared with controls. However, naringin rescued these increases in ROS production, CX3CL1 expression and AKT phosphorylation. Nitric oxide (NO) production and OCR were lower in the high glucose group, and naringin restored the changes induced by high glucose. Molecular docking results suggested that Naringin might interact with the CX3CL1 protein.
Naringin protects HUVECs from high-glucose-induced damage through its antioxidant properties by downregulating CX3CL1 and by improving mitochondrial function.
背景/目的：糖尿病中高血糖诱导内皮损伤已被广泛认可。柚皮苷是一种生物类黄酮。一些研究表明柚皮苷可减轻糖尿病并发症，但柚皮苷改善糖尿病异常的确切机制尚未完全明确。本研究旨在探讨柚皮苷对高糖诱导的人脐静脉内皮细胞（HUVECs）损伤的保护作用。
将HUVECs在有无柚皮苷存在的情况下，分别用高糖或正常培养5天。通过定量实时RT-PCR（qPCR）和蛋白质印迹法检测CX3CL1的表达。用Seahorse Bioscience XF分析仪测量细胞生物能量分析氧消耗率（OCR）。
与对照组相比，高糖培养的HUVECs中活性氧（ROS）生成、CX3CL1表达及AKT磷酸化水平升高。然而，柚皮苷可抑制ROS生成、CX3CL1表达及AKT磷酸化的增加。高糖组一氧化氮（NO）生成和OCR较低，柚皮苷可恢复高糖诱导的变化。分子对接结果表明柚皮苷可能与CX3CL1蛋白相互作用。
柚皮苷通过下调CX3CL1并改善线粒体功能，发挥抗氧化特性，保护HUVECs免受高糖诱导的损伤。
