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Journal Article
Research Support, Non-U.S. Gov't
Protective effects of hyperoside against human umbilical vein endothelial cell damage induced by hydrogen peroxide.
Journal of Ethnopharmacology 2012 January 32
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 (H(2)O(2)), as well as its possible mechanisms.
MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with H(2)O(2) alone or in combination with Hyp. The protective effects of Hyp against H(2)O(2) 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 H(2)O(2) (400μM); 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 H(2)O(2) damage, at least partially, by activating the ERK signaling pathway.
MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with H(2)O(2) alone or in combination with Hyp. The protective effects of Hyp against H(2)O(2) 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 H(2)O(2) (400μM); 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 H(2)O(2) damage, at least partially, by activating the ERK signaling pathway.
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