Based on these results, we propose that P-FA, I-FA, and R-FA protect against cerebral infarction by activating p38 MAPK signaling, and that the attenuating effects of FA treatment on Bax-mediated apoptosis are caused by the upregulation of the p38 MAPK/p90RSK/CREB/Bcl-2 anti-apoptotic pathway in the cortical penumbra 7 d after reperfusion. Here, BCL2 is linked to brain infarction.