Volume 9, Number 2, June 2019
|Number of page(s)||8|
|Published online||24 May 2019|
Gynura bicolor aqueous extract attenuated H2O2 induced injury in PC12 cells
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung 413, Taiwan
2 Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan
* Corresponding author. Department of Food Nutrition and Health Biotechnology, Asia University, No. 500, Liufeng Rd., Wufeng Dist., Taichung 413, Taiwan. E-mail address: firstname.lastname@example.org (Z.-H. Wang)
Accepted: 1 March 2019
Background: Protective effects of Gynura bicolor aqueous extract (GAE) at three concentrations upon nerve growth factor (NGF) differentiated-PC12 cells against H2O2 induced injury were examined.
Methods: NGF differentiated-PC12 cells were treated with GAE at 0.25%, 0.5% or 1%. 100 μM H2O2 was used to treat cells with GAE pre-treatments. After incubating at 37 °C for 12 hr, experimental analyses were processed.
Results: H2O2 exposure decreased cell viability, increased plasma membrane damage, suppressed Bcl-2 mRNA expression and enhanced Bax mRNA expression. GAE pre-treatments reversed these changes. H2O2 exposure reduced mitochondrial membrane potential, lowered Na+-K+-ATPase activity, and increased DNA fragmentation and Ca2+ release. GAE pre-treatments attenuated these alterations. H2O2 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. H2O2 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.
Key words: Gynura bicolor / NGF-PC12 cell / Apoptosis / NF-κB / p38
© Author(s) 2019. This article is published with open access by China Medical University
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