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Gynura bicolor aqueous extract attenuated H(2)O(2) induced injury in PC12 cells

Background: Protective effects of Gynura bicolor aqueous extract (GAE) at three concentrations upon nerve growth factor (NGF) differentiated-PC12 cells against H(2)O(2) induced injury were examined. Methods: NGF differentiated-PC12 cells were treated with GAE at 0.25%, 0.5% or 1%. 100 μM H(2)O(2) wa...

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Detalles Bibliográficos
Autores principales: Yang, Ya-Chen, Wu, Wen-Tzu, Mong, Mei-Chin, Wang, Zhi-Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: EDP Sciences 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6533937/
https://www.ncbi.nlm.nih.gov/pubmed/31124458
http://dx.doi.org/10.1051/bmdcn/2019090212
Descripción
Sumario:Background: Protective effects of Gynura bicolor aqueous extract (GAE) at three concentrations upon nerve growth factor (NGF) differentiated-PC12 cells against H(2)O(2) induced injury were examined. Methods: NGF differentiated-PC12 cells were treated with GAE at 0.25%, 0.5% or 1%. 100 μM H(2)O(2) was used to treat cells with GAE pre-treatments. After incubating at 37 °C for 12 hr, experimental analyses were processed. Results: H(2)O(2) exposure decreased cell viability, increased plasma membrane damage, suppressed Bcl-2 mRNA expression and enhanced Bax mRNA expression. GAE pre-treatments reversed these changes. H(2)O(2) exposure reduced mitochondrial membrane potential, lowered Na(+)-K(+)-ATPase activity, and increased DNA fragmentation and Ca(2+) release. GAE pre-treatments attenuated these alterations. H(2)O(2) stimulated the production of reactive oxygen species (ROS), interleukin (IL)-1beta, IL-6 and tumor necrosis factor-alpha, lowered glutathione content, and reduced glutathione peroxidase (GPX) and catalase activities. GAE pretreatments maintained GPX and catalase activities; and concentration-dependently diminished the generation of ROS and inflammatory cytokines. H(2)O(2) enhanced mRNA expression of nuclear factor kappa (NF-κ) B and p38. GAE pre-treatments decreased mRNA expression of NF-κB and p38. Conclusion: These findings suggested that GAE might be a potent neuronal protective agent.