Puerarin Attenuates LPS-Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

Author:

Chang Xing12ORCID,Zhang Tian3ORCID,Liu Dong4,Meng Qingyan3,Yan Peizheng3ORCID,Luo Duosheng5,Wang Xue6ORCID,Zhou XiuTeng15ORCID

Affiliation:

1. State Key Laboratory of Dao-di Herbs, National Resource Center for Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China

2. Guang’anmen Hospital, Chinese Academy of Traditional Chinese Medicine, Beijing, China

3. Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China

4. Institute of the History of Chinese Medicine and Medical Literature, China Academy of Chinese Medical Sciences, Beijing, China

5. Institute of Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, China

6. School of Business Macau University of Science and Technology, Taipa, Macau, China

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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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