Naringin Protects Against High Glucose-Induced Human Endothelial Cell Injury Via Antioxidation and CX3CL1 Downregulation

• Main Authors: Guilin Li, Yurong Xu, Xuan Sheng, Hua Liu, Jingjing Guo, Jiayue Wang, Qi Zhong, Huaide Jiang, Chaoran Zheng, Mengxia Tan, Shenqiang Rao, Yanling Yu, Yun Gao, Guodong Li, Shangdong Liang, Gaochun Zhu
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2017-08-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Naringin; HUVEC; CX3CL1; ROS; Mitochondria; Oxygen consumption rate
• Online Access: http://www.karger.com/Article/FullText/480215

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). Methods: 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. Results: 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. Conclusion: Naringin protects HUVECs from high-glucose-induced damage through its antioxidant properties by downregulating CX3CL1 and by improving mitochondrial function.