Home HOME General Physiology and Biophysics 2024 General Physiology and Biophysics Vol.43, No.2, p. 153–162, 2024

Journal info


Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.
Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.43, No.2, p. 153–162, 2024

Title: Daidzein protects endothelial cells against high glucose-induced injury through the dual-activation of PPARα and PPARγ
Author: Xuemei Yang, Xinhui Jiang, Changqing Liu, Chuang Yang, Sheng Yao, Hongmei Qiu, Junxia Yang, Ke Wu, Hong Liao, Qingsong Jiang
Abstract: Endothelial damage caused by persistent glucose and lipid metabolism disorders is the main reason of diabetic vascular diseases. Daidzein exerts positive effects on vascular dysfunction. Peroxisome proliferator-activated receptors (PPARs) regulate critically glucose and lipid metabolism. However, the interaction of daidzein to PPARs is still insufficiently explored. In this study, the cell proliferation was detected by EdU. The intrinsic activity and binding affinity of daidzein for human PPARs (hPPARs) were estimated by transactivation reporter gene test and HPLC-UV method, respectively. Daidzein significantly reversed high glucose (HG, at 30 mmol/l)-induced injury in HUVECs, which was inhibited by both PPARα and PPARγ antagonist, but no PPARβ antagonist. Daidzein selectively activated hPPARα and hPPARγ1, but weakly hPPARβ. Additionally, daidzein also bound to both hPPARα and hPPARγ1. The findings suggested that daidzein may be a PPARα and PPARγ dual-agonist. The amelioration of daidzein on HUVECs from hyperglycemia may be mediated by the activation of PPARα and PPARγ receptors.
Keywords: Daidzein — Eendothelial cells — PPARs — Intrinsic activity — Binding affinity
Published online: 07-Mar-2024
Year: 2024, Volume: 43, Issue: 2 Page From: 153, Page To: 162
doi:10.4149/gpb_2023041


download file


© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.