|
| Yiqi-Liangxue Recipe Improves Recovery of InjuredEndothelia by Promoting the Proliferation and Migrationof Vascular Endothelial Cells and BalancingDamage-associated in Flammatory Mediators |
| |
| View Full Text View/Add Comment Download reader |
| DOI：10.15806/j.issn.2311-8571.2016.0007 |
| KeyWord:Yiqi-Liangxue Recipe, PCI, vascular endothelial cells, cell migration, damage-associated mediators |
| Author | Institution |
| Fei Sua |
a.China-Japan friendship Hospital |
| Xiao-Yun Cuib |
b.Dong Fang Hospital, Beijing University of Chinese Medicine |
| Ya-Nan Sunc |
c.Medical Experimental Center, China Academy of Traditional Chinese Medicine |
| Qian Linb |
b.Dong Fang Hospital, Beijing University of Chinese Medicine |
|
| Hits: 1536 |
| Download times: 2212 |
| Abstract: |
| Aim: Yiqi-Liangxue Recipe (YL) is a compound preparation of Chinese medicine used for preventing cardiovascular events after percutaneous
coronary intervention (PCI) (Patent No. 200810240175.4). Maintaining the integrity of endothelia is one of the most effective approaches to
prevent restenosis. Given its clinical protective effects on long-term prognosis, we investigated the mechanisms of YL in protecting vascular
endothelial cells.
Methods: We prepared drugs serum and human umbilical vein endothelial cell (HUVEC) lines. The injured model was employed with
Angiotensin II (Ang II). The YL group was employed with YL treatment. The ARB medicine group was employed with Losartan Potassium
treatment. The combination of Chinese medicine and western medicine (YL+ARB) group was employed with both YL and ARB. The control
group was unemployed with injury and medical treatment. For each group the cell migration rate (CM) and cell proliferation rate (CP) were
measured. The concentration of Nitric Oxide (NO), Reactive Oxygen Species (ROS), Endothelin-1 (ET-1) were assessed. The gene expression
level of ET-1 was observed.
Results: YL+ARB group significantly promoted the speed of the CM/CP of the injured HUVECs. Compared with model group, the
concentration of NO increased after the drug intervention, and the concentration of ET-1 decreased. Compared with YL+ARB group, YL and
ARB group each had the similar weaker effects, but did not have significant difference. The fluorescence of ROS in YL, ARB and YL+ARB group
had no difference because the fluorescence was too strong. Compared with model group, the -2ΔΔCt values were decreased in the YL, ARB and
YL+ARB group. The gene expression level of ET-1 was inhibited after the drug intervention, although with no significant difference.
Conclusion: Treatment with YL ameliorates the injury of vascular endothelial cells and YL+ARB has better curative effect. The mechanisms are
associated with improving the speed of the CM/CP; increasing the release of NO and attenuating the concentration of damage-associated
mediators like ROS, ET-1 and the gene expression level of ET-1. The results suggest that YL may be an option for preventing cardiovascular events
after PCI. |
| Close |
|
|
|