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5-Hydroxymethylfurfural from wine-processed Fructus corni inhibits hippocampal neuron apoptosis

Previous studies have shown that 5-hydroxymethylfurfural, a compound extracted from wine-processed Fructus corni, has a protective effect on hippocampal neurons. The present study was designed to explore the related mechanisms. Our study revealed that high and medium doses (10, 1 μmol/L) of 5-hydrox...

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Detalles Bibliográficos
Autores principales: Gu, Hai, Jiang, Zequn, Wang, Mingyan, Jiang, Haiying, Zhao, Fengming, Ding, Xia, Cai, Baochang, Zhan, Zhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146024/
https://www.ncbi.nlm.nih.gov/pubmed/25206571
http://dx.doi.org/10.3969/j.issn.1673-5374.2013.28.002
Descripción
Sumario:Previous studies have shown that 5-hydroxymethylfurfural, a compound extracted from wine-processed Fructus corni, has a protective effect on hippocampal neurons. The present study was designed to explore the related mechanisms. Our study revealed that high and medium doses (10, 1 μmol/L) of 5-hydroxymethylfurfural could improve the morphology of H(2)O(2)-treated rat hippocampal neurons as revealed by inverted phase-contrast microscopy and transmission electron microscopy. MTT results showed that incubation with high and medium doses of 5-hydroxymethylfurfural caused a significant increase in the viability of neuronal cells injured by H(2)O(2). Flow cytometry assays firmed that H(2)O(2) could induce cell apoptosis, while high and medium doses of 5-hydroxymethylfurfural had a visible protective effect on apoptotic rat hippocampal neurons. Real-time PCR and western blot analysis showed that high and medium doses of 5-hydroxymethylfurfural prevented H(2)O(2)-induced up-regulation of p53, Bax and caspase-3 and an-tagonized the down-regulation of Bcl-2 induced by H(2)O(2) treatment. These results suggested that 5-hydroxymethylfurfural could inhibit apoptosis of cultured rat hippocampal neurons injured by H(2)O(2) via increase in Bcl-2 levels and decrease in p53, Bax and caspase-3 protein expression levels.