期刊
MOLECULES
卷 26, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/molecules26010090
关键词
oxidative stress; ferulic acid; apoptosis; cell signaling
资金
- Japan Society for the Promotion of Science (JSPS) KAKENHI [18K08984]
- Scholarship Fund forWomen Researchers from Promotion and Mutual Aid Corporation for Private Schools of Japan
Ferulic acid has antioxidant and anti-apoptotic effects in PC12 cells, protecting neurons from damage by inhibiting apoptosis and reducing reactive oxygen species production. It regulates protein phosphorylation, apoptosis-related proteins, and microRNA expression to mitigate oxidative stress induced by H2O2 in rat pheochromocytoma cells.
Ferulic Acid (FA) is a highly abundant phenolic phytochemical which is present in plant tissues. FA has biological effects on physiological and pathological processes due to its anti-apoptotic and anti-oxidative properties, however, the detailed mechanism(s) of function is poorly understood. We have identified FA as a molecule that inhibits apoptosis induced by hydrogen peroxide (H2O2) or actinomycin D (ActD) in rat pheochromocytoma, PC12 cell. We also found that FA reduces H2O2-induced reactive oxygen species (ROS) production in PC12 cell, thereby acting as an anti-oxidant. Then, we analyzed FA-mediated signaling responses in rat pheochromocytoma, PC12 cells using antibody arrays for phosphokinase and apoptosis related proteins. This FA signaling pathway in PC12 cells includes inactivation of pro-apoptotic proteins, SMAC/Diablo and Bad. In addition, FA attenuates the cell injury by H2O2 through the inhibition of phosphorylation of the extracellular signal-regulated kinase (ERK). Importantly, we find that FA restores expression levels of brain-derived neurotrophic factor (BDNF), a key neuroprotective effector, in H2O2-treated PC12 cells. As a possible mechanism, FA increases BDNF by regulating microRNA-10b expression following H2O2 stimulation. Taken together, FA has broad biological effects as a neuroprotective modulator to regulate the expression of phosphokinases, apoptosis-related proteins and microRNAs against oxidative stress in PC12 cells.
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