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Allicin prevents H(2)O(2)-induced apoptosis of HUVECs by inhibiting an oxidative stress pathway
BACKGROUND: Allicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function. METHODS: To investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs)...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4158076/ https://www.ncbi.nlm.nih.gov/pubmed/25174844 http://dx.doi.org/10.1186/1472-6882-14-321 |
Sumario: | BACKGROUND: Allicin, a primary ingredient of garlic, has been proposed to possess cardioprotective properties, which are commonly mediated by improved endothelial function. METHODS: To investigate the effect and mechanism of allicin on the apoptosis of human umbilical vein endothelial cells (HUVECs), we used Propidium iodide (PI) staining and Annexin V/ PI staining assays to establish a model of oxidative stress apoptosis induced by H(2)O(2). MTT, RT-PCR and western-blot assays were used to detect the effects and mechanism of allicin on the model. RESULTS: PI staining, Annexin V/ PI staining assays and morphological assessment suggest that the cell death induced by 0.5 mM H(2)O(2) is primarily apoptotic. Conversely, allicin reverses the effect of H(2)O(2) on cell death, suggesting a role in protecting HUVECs from apoptosis. We demonstrated that H(2)O(2) activates PARP cleavage, reduces pro-Caspase-3 levels and activates Bax expression; however, allicin inhibits each of these apoptotic signaling indicators. Allicin also reduces the levels of malondialdehyde and increases the levels of superoxide dismutase, nitric oxide release and endothelial nitric oxide synthase mRNA, but has no significant effect on inducible nitric oxide synthase mRNA levels. CONCLUSION: These results demonstrate that allicin has powerful effects in protecting HUVECs from apoptosis and suggest that protection occurs via a mechanism involving the protection from H(2)O(2)-mediated oxidative stress. |
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