Background
Protocatechuic aldehyde (PA) extracts from S. miltiorrhiza, which anti-oxidative and anti-inflammatory functions have been certified in diverse diseases. Nonetheless, the influence of PA in spinal cord injury (SCI) is still hazy. The research probed the function of PA in hydrogen peroxide (H2O2)-damaged PC12 cells.
Conclusions
The results disclosed the protective impacts of PA on PC12 cells to resist H2O2-provoked damage. MEG3, Wnt/β-catenin and PTEN/PI3K/AKT pathways joined in adjusting the activity of PA in H2O2-damaged PC12 cells.
Methods
The disparate dosages of H2O2 (0-400 µM) or PA (0-2 µM) were applied for stimulating PC12 cells, and subsequently cell viability, apoptosis, apoptosis- and autophagy-correlative factors were evaluated. After pc-MEG3 transfection, functions of MEG3 overexpression in H2O2 and/or PA-managed PC12 cells were reassessed. Western blot was conducted to determine Wnt/β-catenin and PTEN/PI3K/AKT pathways.
Results
H2O2 stimulation clearly triggered PC12 cell damage via prohibiting cell viability and accelerating apoptosis and autophagy. But, PA management mitigated H2O2-triggered PC12 cells damage. Down-regulated MEG3 triggered by PA was presented in H2O2-managed cells. What's more, overexpressed MEG3 dramatically overturned the influences of PA in H2O2-damaged PC12 cells. Beyond that, PA activated Wnt/β-catenin and PTEN/PI3K/AKT via repression of MEG3 in H2O2-managed PC12 cells.Conclusions: The results disclosed the protective impacts of PA on PC12 cells to resist H2O2-provoked damage. MEG3, Wnt/β-catenin and PTEN/PI3K/AKT pathways joined in adjusting the activity of PA in H2O2-damaged PC12 cells.