Protective Effect of Ferulic Acid against Hydrogen Peroxide Induced Apoptosis in PC12 Cells.
Hironao NakayamaMasako NakaharaErina MatsugiMidori SodaTomoka HattoriKoki HaraAyuki UsamiChiaki KusumotoShigeki HigashiyamaKiyoyuki KitaichiPublished in: Molecules (Basel, Switzerland) (2020)
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.
Keyphrases
- oxidative stress
- hydrogen peroxide
- induced apoptosis
- endoplasmic reticulum stress
- signaling pathway
- cell death
- poor prognosis
- diabetic rats
- reactive oxygen species
- single cell
- nitric oxide
- cell cycle arrest
- dna damage
- pi k akt
- anti inflammatory
- gene expression
- cell therapy
- cell proliferation
- epithelial mesenchymal transition
- binding protein
- cerebral ischemia
- high glucose
- endothelial cells
- bone marrow
- protein kinase
- high density
- type iii