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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Stroke. 2013 Jul 23;44(9):10.1161/STROKEAHA.113.001530. doi: 10.1161/STROKEAHA.113.001530

Figure 5. Cilostazol-induced OPC proliferation/differentiation in vitro.

Figure 5

A. Western blot images using samples from cultured rat OPCs with 7-day CoCl2 treatment. HIF1α is a marker for hypoxic conditions, NG2 is a marker for OPCs, GST-pi and MBP are markers for mature OLs, and β-actin is an internal control. B. LDH assays showed that 0.01 to 1 μM of CoCl2 (7-day treatment) did not induce cell death in our OPCs. N=6. Values are mean ± SD. C. Representative images of NG2, GST-pi and MBP staining in cultured rat OPCs at day 7 after the CoCl2 treatment with or without cilostazol. Bar = 25 μm. D. Representative images of pCREB, PDGFR-α and CNPase staining in cultured rat OPCs at day 7 after CoCl2 treatment with or without cilostazol. Bar = 25 μm.