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Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide
Authors:Li Zi-lin  Liu Jin-cheng  Hu Jing  Li Xiao-qiang  Wang Si-wang  Yi Ding-hua  Zhao Ming-gao
Affiliation:a Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China
b School of Pharmacy, Fourth Military Medical University, Xi’an 710032, China
c Institute of Pharmaceutical Research, Fourth Military Medical University, Xi’an 710032, China
d Department of Cardiothoracic Surgery, PLA 452 Hospital, Chengdu 610061, Sichuan, China
e Department of Pharmacy, General Hospital of Lanzhou Command, PLA, Lanzhou 730050, China
Abstract:

Ethnopharmacological relevance

Hyperoside (Hyp) is a flavonoid compound isolated from Rhododendron ponticum L. leaves that elicits vascular protective effects in vitro. Treatment with Hyp has been found to attenuate endothelial cell damage induced by oxidative stress, but its mechanisms of action remain unclear.This study investigated the action of Hyp in an endothelial injury model induced by hydrogen peroxide (H2O2), as well as its possible mechanisms.

Materials and methods

Human umbilical vein endothelial cells (HUVECs) were treated with H2O2 alone or in combination with Hyp. The protective effects of Hyp against H2O2 were evaluated, and the activation of extracellular signal-regulated protein kinase (ERK) in Hyp was assayed in HUVECs.

Results

Loss of cell viability as well as excessive cell apoptosis and death were observed in HUVECs after 18 h of challenge with H2O2 (400 μM); however, both cell apoptosis and death were attenuated in the Hyp-pretreated cells. Western blot analysis revealed that Hyp increased the expression of Bcl-2 but decreased that of Bax. In addition, Hyp induced the phosphorylation of ERK1/2 in HUVECs.

Conclusion

These observations provide preliminary evidence that Hyp protects HUVECs against H2O2 damage, at least partially, by activating the ERK signaling pathway.
Keywords:Hyperoside   Apoptosis   Endothelium   ERK   Oxidative stress
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