Ginkgo biloba extract alleviates oxygen and glucose deprivation/reperfusion injury in cardiac microvascular endothelial cells by regulating NF-κB and CHOP signaling pathways through SIRT6
10.12025/j.issn.1008-6358.2025.20241262
- VernacularTitle:银杏叶提取物通过SIRT6调控NF-κB和CHOP信号通路改善氧糖剥夺/复氧诱导的心脏微血管内皮细胞损伤
- Author:
Mukaddas ABDURAHMAN
1
;
Zhenyang GUO
1
;
Junbo GE
1
;
Hua LI
1
Author Information
1. Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
- Publication Type:Originalarticle
- Keywords:
Ginkgo biloba extract;
cardiac microvascular endothelial cells;
oxygen and glucose deprivation/reperfusion;
endoplasmic reticulum stress;
SIRT6
- From:
Chinese Journal of Clinical Medicine
2025;32(1):46-57
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of Ginkgo biloba extract (GBE) on cardiac microvascular endothelial cells (CMECs) under oxygen and glucose deprivation/reperfusion (OGD/R) condition and its molecular mechanisms. Methods An OGD/R-induced injury model was established in CMECs. According to different intervention, CMECs were divided into four groups: normoxia blank control group (WT group), WT + GBE group, OGD/R group, and OGD/R + GBE group. Cell apoptosis was detected by flow cytometry technology in each group. The oxidative stress was examined by MitoSox staining. The migration abilities were measured by scratch assay. The expressions of PERK/eIF2α/CHOP, nuclear factor kappa B (NF-κB), and endothelial cell function markers were detected by Western blotting. Results Compared with the WT group, the endothelial cell apoptosis level in the OGD/R group significantly increased, with markedly aggravated cellular dysfunction. The expressions of p-NF-κB, vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1) were significantly upregulated (P＜0.05), and the activation of the CHOP signaling pathway was notably enhanced (P＜0.05). After intervention with GBE, endothelial cell apoptosis caused by OGD/R injury was significantly reduced, oxidative stress and inflammation levels were markedly downregulated, and the expression of p-NF-κB was considerably decreased (P＜0.05), while the CHOP signaling pathway was notably inhibited (P＜0.05). Furthermore, it was found that GBE could promote expression of SIRT6 to regulate the above molecules, thereby alleviating cardiac microvascular endothelial cell injury under OGD/R condition. On the contrary, when SIRT6 was knocked down, the protective effects were significantly reduced. Conclusions GBE improves endothelial cell dysfunction, endoplasmic reticulum stress, and endothelial cell apoptosis caused by OGD/R injury by promoting the expression of SIRT6 protein, thus regulating the NF-κB inflammatory pathway and CHOP signaling pathway.
