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Chinese Journal of Pathophysiology ; (12): 1180-1188, 2016.
Artigo em Chinês | WPRIM | ID: wpr-496561

RESUMO

AIM:To study the protective effect of procyanidin single active ingredient B2 (PC-B2) on human endothelial progenitor cells ( EPCs) stimulated with high glucose.METHODS: The human EPCs were isolated from pe-ripheral blood of healthy people and identified.The EPCs were divided into control group (PBS treatment), hypertonic control group (25 mmol/L mannitol treatment), high glucose (30 mmol/L) group, and different concentrations (2, 10 and 50 mg/L) of PC-B2+30 mmol/L glucose groups.The viability of EPCs was detected by CCK-8 assay.The levels of LDH, MDA, SOD and GSH in the EPCs were detected.The changes of NO, ET-1, ICAM-1 and VCAM-1 in the EPCs cultured medium were measured by ELISA.The cell apoptotic rate and reactive oxygen species ( ROS) in the EPCs were analyzed by flow cytometry.The expression of VEGF and VEGFR-2 in the EPCs were determined by Western blot.RE-SULTS:Compared with control group, the viability of human EPCs was decreased significantly in 30 mmol/L glucose group (P cantly (P<0.05), but SOD and GSH activity and NO production were decreased significantly (P<0.05).The ROS and cell apoptotic rate were increased significantly (P<0.05).The expression of VEGF and VEGFR-2 in the EPCs were de-creased (P<0.05).When human EPCs were treated with different concentrations of PC-B2 and 30 mmol/L glucose, the viability was obviously rebounded (P<0.05), the LDH leakage, MDA content and the releases of ET-1, ICAM-1 and VCAM-1 were decreased gradually (P<0.05), the SOD, GSH activity and NO production were increased significantly (P<0.05), the ROS and cell apoptotic rate were decreased significantly (P<0.05), and the expression of VEGF and VEGFR-2 in the EPCs was increased gradually ( P <0.05 ) .CONCLUSION: PC-B2 enhances the viability of human EPCs under high glucose condition, reduces high glucose-induced oxidative damage, restores the EPCs normal function, and reduces the releases of inflammatory cytokines and apoptosis, thus playing a protective effect on human EPCs through inducing the expression of VEGF and VEGFR-2.

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