Protocatechuic aldehyde activates GPER1 as G1 agonist to attenuate atherosclerosis

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 818-841-Diabetes Pathophysiology & Complications
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-832
Byung Soo Kong*, Yoon Hee Cho and Eun Jig Lee
Yonsei University College of Medicine, Seoul, South Korea
Protocatechuic aldehyde activates GPER1 as G1 agonist to attenuate atherosclerosis


Byung Soo Kong1, Yoon Hee Cho1, and Eun Jig Lee 1

1Endocrinology, Severance Integrative Research Institute for Cerebral & Cardiovascular Diseases, Yonsei University College of Medicine, Seoul, Korea


Protocatechuic aldehyde (PCA) is a single compound found in aqueous extract of Salvia Miltiorrhiza that have recently been reported for its antioxidative effects in atherosclerosis. Numerous studies suggest that two estrogen receptors, ER α and ER β, have beneficial cardiovascular effects. However, effects of G-protein coupled estrogen receptor (GPER-1), the third membrane bound estrogen receptor, on atherosclerosis are not well understood. Here, we report that PCA reduces vascular inflammation through increasing GPER-1 expression at mRNA and protein level in the similar manner as GPER-1 agonist, G1.

In order to find out the anti-atherogenic effects of PCA, HUVECs were pretreated with PCA and G1 and then, tumor necrosis factor alpha (TNF-α) was given. PCA and G1 prevented the TNF-α stimulated inflammatory process by reducing VCAM-1, ICAM-1, and HIF1-α expression in HUVECs. Subsequently, reduced phosphorylation of p-38 MAPK and Nf-kB were observed by treatment of PCA and G1.

In addition, HUVECs were treated with G15, an antagonist of GPER-1, and its GPER-1 gene was silenced to elucidate the effects of GPER-1 and PCA on endothelial cell inflammation. Increased expression of VCAM-1 and ICAM-1 were observed from both groups. However, PCA and G1 decreased the expression of these adhesion molecules. Our results demonstrated that PCA has anti-atherogenic effects by activating GPER-1 as G1 and by restoring GPER-1 expression inhibited by siRNA and G15.

Nothing to Disclose: BSK, YHC, EJL

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