Curculigoside attenuates human umbilical vein endothelial cell injury induced by H2O2
| Autor: | Hao Zhu Chen, Yun Kai Wang, Ye Wu, Zhao Quan Huang, Mao Wei, Ya Jun Hong, Rui Zhen Chen |
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| Rok vydání: | 2010 |
| Předmět: |
Umbilical Veins
Endothelium Cell Survival Biology Pharmacology medicine.disease_cause Nitric Oxide Benzoates Umbilical vein Antioxidants Cell Line Curculigo Glucosides Drug Discovery medicine Humans chemistry.chemical_classification Curculigoside Reactive oxygen species Endothelial Cells Hydrogen Peroxide biology.organism_classification Curculigo orchioides Endothelial stem cell Oxidative Stress medicine.anatomical_structure Biochemistry chemistry Human umbilical vein endothelial cell Endothelium Vascular Lipid Peroxidation Reactive Oxygen Species Oxidative stress Rhizome |
| Zdroj: | Journal of ethnopharmacology. 132(1) |
| ISSN: | 1872-7573 |
| Popis: | Aim of the study Vessel endothelium injury caused by reactive oxygen species (ROS) including H 2 O 2 plays a critical role in the pathogenesis of cardiovascular disorders. Therefore, agents or antioxidants that can inhibit production of ROS has highly clinical values in cardiovascular therapy. Curculigoside is the major bioactive compounds present in Curculigo orchioides , and possess potent antioxidant properties against oxidative stress insults through undefined mechanism(s). The present study was designed to test the hypothesis that curculigoside can inhibit H 2 O 2 -induced injury in human umbilical vein endothelial cells. Materials and methods Human umbilical vein endothelial cells (HUVECs) were treated with curculigoside in the presence/absence of hydrogen peroxide (H 2 O 2 ). The protective effects of curculigoside OP-D against H 2 O 2 were evaluated. Results HUVECs incubated with 400 μM H 2 O 2 had significantly decreased the viability of endothelial cells, which was accompanied with apparent cells apoptosis, the activation of caspase-3 and the upregulation of p53 mRNA expression. In addition, H 2 O 2 treatment induced a marked increase of MDA, LDH content and in intracellular ROS, decreased the content of nitric oxide (NO) and GSH-Px activities in endothelial cells. However, pretreatment with 0.5.5,10 μM curculigoside resulted in a significant recovery from H 2 O 2 -induced cell apoptosis. Also, it decreased other H 2 O 2 -induced damages in a concentration-dependent manner. Furthermore, pretreatment with curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H 2 O 2 -induced cell apoptosis. Conclusion The present study shows that curculigoside can protect endothelial cells against oxidative injury induced by H 2 O 2 , suggesting that this compound may constitute a promising intervention against cardiovascular disorders. |
| Databáze: | OpenAIRE |
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