Chlorpromazine and Promethazine (C+P) Reduce Brain Injury after Ischemic Stroke through the PKC-δ/NOX/MnSOD Pathway

Figure 1

C+P lessened postischemic neurologic damage. (a) Alterations in body temperature post C+P administration at various points in time in 2-hour MCAO and after reperfusion (0–24 hours). Baseline temperatures were determined just before MCAO. Reperfusion was followed by C+P administration. ANOVA analyses specified that C+P significantly decreased body temperatures as early as 5 minutes and lasting up to 6 hours after the I/R onset (). (b) TTC stains showcase infarction volumes in MCAO rats regardless of C+P treatment at 48 hours of reperfusion. C+P administration or administration of the PKC-δ/NOX inhibitor significantly decreased infarct volumes (). (c) Neurologic deficits were determined using 5- or 12-point scoring systems at 48 hours of reperfusion. C+P administration or the administration of the PKC-δ/NOX inhibitor significantly reduced neurological deficits in all groups except those in the temperature-controlled C+P group, for which there was no effect on the 5-point scoring system (). (d) Cell death was significantly higher at 6 and 24 hours of reperfusion, demonstrated by ELISA. With C+P at 6 and 24 hours of reperfusion, cell death was significantly reduced. Administration of the PKC-δ/NOX inhibitor also suppressed cell death except in the NOX inhibitor group at 6 hours of reperfusion (). (e) Apoptotic cell death was significantly reduced with C+P administration regardless of temperature control at 24 hours of reperfusion, shown using the TUNEL assay (). . versus the sham group; ^#, ^##, and ^### versus the I/R group. Results are shown as .

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