Salidroside attenuates high glucose-induced apoptosis in human umbilical vein endothelial cells via activating the Ca2+/CaM/CAMK Ⅱ δ/eNOS pathway
10.3760/cma.j.issn.0253-3758.2014.04.013
- VernacularTitle:红景天苷通过激活钙离子/钙调蛋白/钙调蛋白激酶δ/内皮型一氧化氮合酶通路抑制高糖对人脐静脉内皮细胞的损伤
- Author:
Ziwei CHEN
1
;
Xiang WU
Author Information
1. 226001,南通大学附属医院心血管内科
- Keywords:
Blood vessels;
Endothelial cells;
Hyperglycemia;
Salidroside
- From:
Chinese Journal of Cardiology
2014;42(4):327-333
- CountryChina
- Language:Chinese
-
Abstract:
Objective Endothelial oxidative stress plays an important role in the pathogenesis of cardiovascular disease.Salidroside,a phenylpropanoid glycoside isolated from Rhodiola rosea L,could e xert potent antioxidant properties.In this study,we investigated the protective effects,and related mechanism of salidroside against high glucose (33 mmol/L)-induced cell damage in human umbilical vein endothelial cells (HUVECs).Methods HUVECs were cultured in normal glucose (5.5 mmol/L),high glucose (33 mmol/L),high salidroside (10 μg/ml + 33 mmol/L glucose),moderate salidroside (4 μg/ml + 33 mmol/L glucose),low salidroside (1 μg/ml + 33 mmol/L glucose) and very low salidroside (0.1 μg/ml + 33 mmol/L glucose) for 48 h.Cell viability,the level of malondialdehyde (MDA),reactive oxygen species (ROS),nitric oxide (NO),[Ca2 +] i,calmodulin (CaM),calmodulin-dependent kinase (CaMK) Ⅱ δ,endothelial nitric oxide synthase(eNOS),active caspase-3 protein expression and eNOS ser 1177 phosphorylation of HUVECs post various treatments were measured.The cell viability was assessed with MTT assay,and the level of ROS,and [Ca2 +] i was analyzed using flow cytometry.Nitric oxide and MDA was detected by Nitric Oxide Assay Kit and MDA Assay Kit.Western blot was performed to detect the protein expressions of eNOS,active caspase-3 and eNOS ser 1177 phosphorylation.Results Comparing to the normal glucose group,high glucose treatment increased the cell damage,the level of NO and [Ca2 +] i (P ＜ 0.05),downregulated CAMK Ⅱ δ,eNOS expression and eNOS ser 1177 phosphorylation(P ＜ 0.05),elevated the concentration of MDA and ROS (P ＜ 0.05) in HUVECs.Salidroside treatment significantly attenuated high glucose-induce cell damage on cultured HUVECs in a dose-dependent manner.Comparing to the high glucose group,10 μg/ml Salidroside significantly increased cell viability(P ＜ 0.05),inhibited high glucose-induced release of MDA,generation of ROS,active caspase 3 protein expression (P ＜ 0.05),upregulated the release of nitric oxide and [Ca2 +] i by HUVECs(P ＜ 0.05),enhanced CaM,CAMK Ⅱ δ,eNOS expression and eNOS ser 1177 phosphorylation in HUVECs(P ＜ 0.05).Conclusions These findings suggeste that salidroside could attenuate high glucose induced apoptosis in HUVEC,partly through activating the Ca2+/CaM/CAMK Ⅱ δ/eNOS pathway.
