Abstract
Atherosclerosis is closely associated with the inflammatory reaction of vascular endothelial cells. Puerarin (Pue), the main active component isolated from the rhizome of Pueraria lobata, is an isoflavone compound with potent antioxidant properties. Although Pue exhibits promising antiatherosclerotic pharmacological effects, only a few studies have reported its protective effect on endothelial cells. This study found that Pue could partly regulate mitochondrial function in human umbilical vein endothelial cells (HUVECs) and reduce or inhibit lipopolysaccharide-induced inflammatory reactions and oxidative stress injury in HUVECs, likely via mitochondrial quality control. Furthermore, the protective effect of Pue on HUVECs was closely related to the SIRT-1 signaling pathway. Pue increased autophagy and mitochondrial antioxidant potential via increased SIRT-1 expression, reducing excessive production of ROS and inhibiting the expression of inflammatory factors and oxidative stress injury. Therefore, Pue may improve mitochondrial respiratory function and energy metabolism, increasing the vulnerability of HUVECs to an inflammatory state.
Highlights
Atherosclerosis (AS) is a protective response to arterial wall endothelium and smooth muscle injury, including the formation of lipid streaks and fiber injury, and is always accompanied by an inflammatory reaction [1, 2]
A human umbilical vein endothelial cells (HUVECs) inflammatory model was established by stimulating HUVECs with LPS to preliminarily confirm the effect of Pue on the function of HUVECs in an LPS-mediated inflammatory state
The analysis showed that LPS increased apoptosis levels of HUVECs, but 100 mg/L Pue inhibited the apoptosis (Figures 1(c) and 1(d))
Summary
Atherosclerosis (AS) is a protective response to arterial wall endothelium and smooth muscle injury, including the formation of lipid streaks and fiber injury, and is always accompanied by an inflammatory reaction [1, 2]. Mitochondria are important mediators in cells, and mitochondrial dysfunction can indirectly activate a variety of inflammatory signal transduction pathways, leading to tissue and cell damage. The oxidative effect of mitochondrial ROS on mitochondrial DNA during activation of NLRP3 leads to a partial inflammatory potential of free circulating mitochondrial DNA This shows that oxidative stress and the mitochondrial pathway can affect MQC and endothelial cell inflammatory responses in an interdependent manner. Other studies have shown that Pue can reduce vascular endothelium injury and the expression of IL-1β, IL-8, ICAM-1, and PAI-1 in the supernatant of human umbilical vein endothelial cells (HUVECs) stimulated with LPS. We investigated whether the inhibitory effect of Pue on LPSinduced endothelial cell inflammation and oxidative stress injury was mediated by mitochondria
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