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SB220025 a p38 inhibitor mediates neuroprotection by inhibiting transcriptional activation and apoptosis in focal cerebral ischemia

In the present study [5‐(2‐amino‐4‐pyrimidinyl)‐4‐(fluorophenyl)‐1‐(4piperidinyl)imidazole)] (SB220025) a p38 inhibitor was evaluated for its neuroprotective efficacy in transient focal cerebral ischemia (FCI) model. FCI was induced in rat by occluding middle cerebral artery for 2 h followed by 70 h of reperfusion. IR insult resulted in a prominent infarction (188.5±25.7 mm3) and edema (115.1±28.1 mm3) in the ipsilateral hemisphere of brain. Severe motor dysfunction was also observed in ischemic rats (median cumulative deficit score 9.0±1.8). The temporal pattern of p38 activation was found to be biphasic in nature. IR insult also resulted in an intense NFκB binding and apoptosis mediated neuronal loss. Intravenous administration of SB220025 (0.5 and 1 mg/kg) reduced the extent of infarct volume. SB220025 (1 mg/kg) treatment resulted in a statistically significant improvement in neurological score. Treatment with SB220025 (1 mg/kg) also resulted in a statistically significant decrease in TNFα abundance, number of TUNEL positive cells. These results demonstrate that SB220025 is an efficacious neuroprotective agent which mediates its effect at least in part by inhibiting TNFα abundance and apoptosis mediated neuronal loss.