Abstract: Objective To investigate the effects of minocycline in promoting the survival of pheochromocytoma (PC12) cells
exposed to oxygen glucose deprivation (OGD) and explore the underlying mechanisms. Methods An in vitro cell model of
cerebral ischemia was established by OGD for 6 h in PC12 cells with pretreatment with minocycline or an ERK1/2 inhibitor. At
24 h after OGD injury, the cells were evaluated for cell viability by MTT assay and expressions of heme oxygenase-1 (HO-1)
and phospholylated extracellular signal-regulated protein kinase 1/2 (ERK1/2) by Western blotting. Results The cell viability
decreased dramatically following OGD. Pretreatment with minocycline (0.1-10 μmol/L) induced a significant increase in the
cell viability after OGD and caused up-regulation of HO-1 protein and enhanced ERK1/2 phospholylation, and the effects were
especially obvious with 1 μmol/L minocycline and were abolished by inhibition of ERK1/2 activity with U0126 (10 μmol/L).
Conclusion Minocycline can protect PC12 cells against OGD-induced toxicity by up-regulating HO-1 protein expression
through ERK1/2 signaling pathways.