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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: J Neurochem. 2015 Jun 1;134(3):463–470. doi: 10.1111/jnc.13152

Figure 2.

Figure 2

Rosiglitazone protects Neuro2A cells against oxidative stress in an NF-α1-dependent manner. (A) Representative Western blot and (B, C) quantification showing increased NF-α1 (A, B) and BCL-2 (A, C) protein levels in Neuro2a cells treated with vehicle (Veh) or 1 μM rosiglitazone (Rosi) for 24 h. (n = 6/group; values are mean ±SEM, **p<0.01, ***p<0.001, t-test). (D) Neuro2A cells were transfected with siScr or siNF-α1 for 24 h and then treated with 1 μM Rosi or vehicle for 24 h, then 100 μM H2O2 or vehicle was added to the cells for an additional 24 h. The LDH release assay showed Rosi inhibited H2O2 induced cell cytotoxicity in siScr treated Neuro2A cells but not in siNF-α1 treated cells. n=5/group; values are mean ±SEM, one way ANOVA for siScr [treatment effect: F(3, 16)=60.11, p<0.001]; for siCPE [treatment effect: F(3, 16)=121.9, p<0.001], followed by Tukey test. *p <0.05, H2O2 group compared to Rosi + H2O2 group.