Panax Notoginseng Saponin Attenuates Gastric Mucosal Epithelial Cell Injury Induced by Dual Antiplatelet Drugs through COX and PI3K/Akt/ VEGF-GSK-3β-RhoA Network Pathway.
10.1007/s11655-021-2854-3
- Author:
Ming-Ming WANG
1
;
Mei XUE
2
;
Zhong-Hai XIN
3
;
Yan-Hui WANG
1
;
Rui-Jie LI
1
;
Hong-Yan JIANG
4
;
Da-Zhuo SHI
2
Author Information
1. Beijing First Hospital of Integrated Chinese and Western Medicine, Beijing, 100039, China.
2. Center for Cardiovascular Disease, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
3. Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, 100102, China.
4. Beijing First Hospital of Integrated Chinese and Western Medicine, Beijing, 100039, China. billhappy@yeah.net.
- Publication Type:Journal Article
- Keywords:
PI3K;
Panax notoginseng saponins;
cyclooxygenase;
dual antiplatelet;
permeability
- MeSH:
Cyclooxygenase 1;
Epithelial Cells/metabolism*;
Glycogen Synthase Kinase 3 beta;
Humans;
Panax notoginseng;
Phosphatidylinositol 3-Kinases/metabolism*;
Platelet Aggregation Inhibitors;
Proto-Oncogene Proteins c-akt/metabolism*;
Saponins/pharmacology*;
Vascular Endothelial Growth Factor A;
rhoA GTP-Binding Protein
- From:
Chinese journal of integrative medicine
2021;27(11):819-824
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To elucidate the underlying mechanism of Panax notoginseng saponin (PNS) on gastric epithelial cell injury and barrier dysfunction induced by dual antiplatelet (DA).
METHODS:Human gastric mucosal epithelial cell (GES-1) was cultured and divided into 4 groups: a control, a DA, a PNS+DA and a LY294002+PNS+DA group. GES-1 apoptosis was detected by flow cytometry, cell permeability were detected using Transwell, level of prostaglandins E2 (PGE2), 6-keto-prostaglandin F1α (6-keto-PGF1α) and vascular endothelial growth factor (VEGF) in supernatant were measured by enzyme linked immunosorbent assay (ELISA), expression of phosphatidylinositide 3-kinase (PI3K), phosphorylated-PI3K (p-PI3K), Akt, phosphorylated-Akt (p-Akt), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), glycogen synthase kinase-3β (GSK-3β) and Ras homolog gene family member A (RhoA) were measured by Western-blot.
RESULTS:DA induced apoptosis and hyper-permeability in GES-1, reduced supernatant level of PGE2, 6-keto-PGF1α and VEGF (P<0.05). Addition of PNS reduced the apoptosis of GES-1 caused by DA, restored the concentration of PGE2, 6-keto-PGF1α and VEGF (P<0.05). In addition, PNS attenuated the alteration of COX-1 and COX-2 expression induced by DA, up-regulated p-PI3K/p-Akt, down-regulated RhoA and GSK-3β. LY294002 mitigated the effects of PNS on cell apoptosis, cell permeability, VEGF concentration, and expression of RhoA and GSK-3β significantly.
CONCLUSIONS:PNS attenuates the suppression on COX/PG pathway from DA, alleviates DA-induced GES-1 apoptosis and barrier dysfunction through PI3K/Akt/ VEGF-GSK-3β-RhoA network pathway.
