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. Author manuscript; available in PMC: 2012 May 1.
Published in final edited form as: Neurobiol Dis. 2011 Jul 2;44(1):142–151. doi: 10.1016/j.nbd.2011.06.016

Fig. 7.

Fig. 7

(A) Cells were exposed for 72 h to control conditions or MCM10 in the presence or absence of VPA (1 mM). Next, cells were exposed to hydrogen peroxide (250 µM) for 3 h and cell death was assessed by measuring the LDH released into the bathing medium. Long-term exposure to MCM10 rendered astrocyte-rich cultures more susceptible to oxidative stress induced by hydrogen peroxide, showing higher levels of cell loss. This effect was partially reversed by the treatment with VPA (1 mM). The results shown are the mean ± SEM. Statistics: ***p<0.005 vs control; ###p<0.005 vs MCM10. (B) Cells were exposed for 72 h to control conditions or MCM10 in the presence or absence of TSA (10 nM). Next, cells were exposed to hydrogen peroxide (250 µM) for 3 h and cell death was assessed by measuring the LDH released into the bathing medium. Prolonged exposure to MCM10 rendered astrocyte-rich cultures more susceptible to oxidative stress induced by hydrogen peroxide, showing higher levels of cell loss. This effect was partially reversed by the treatment with TSA (10 nM). The results shown are the mean ± SEM. Statistics: ***p<0.005 vs control; ###p<0.005 vs MCM10.