RETRACTED: Puerarin Attenuates LPS-Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control (Retracted article)

被引:39
作者
Chang, Xing [1 ,2 ]
Zhang, Tian [3 ]
Liu, Dong [4 ]
Meng, Qingyan [3 ]
Yan, Peizheng [3 ]
Luo, Duosheng [5 ]
Wang, Xue [6 ]
Zhou, XiuTeng [1 ,5 ]
机构
[1] China Acad Chinese Med Sci, Natl Resource Ctr Chinese Mat Med, State Key Lab Dao di Herbs, Beijing, Peoples R China
[2] Chinese Acad Tradit Chinese Med, Guanganmen Hosp, Beijing, Peoples R China
[3] Shandong Univ Tradit Chinese Med, Jinan, Shandong, Peoples R China
[4] China Acad Chinese Med Sci, Inst Hist Chinese Med & Med Literature, Beijing, Peoples R China
[5] Guangdong Pharmaceut Univ, Inst Chinese Med, Guangzhou, Peoples R China
[6] Macau Univ Sci & Technol, Sch Business, Taipa, Macao, Peoples R China
基金
中国国家自然科学基金;
关键词
D O I
10.1155/2021/6659240
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页数:14
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