Figure 6.

Pharmacological blockade of cytosolic phospholipase A₂ (cPLA₂) with AACOCF3 reduced cPLA₂ activity, membrane injury, and inflammation induced by spinal cord injury (SCI). (A–C) AACOCF3 significantly inhibited an increase of cPLA₂ (A) and total PLA₂ (C) activities induced by SCI at 24 hours postinjury. However, AACOCF3 did not significantly affect SCI-induced Ca²⁺-independent PLA₂ (iPLA₂) activity (B). (D) AACOCF3 also inhibited an increase of prostaglandin E₂ (PGE₂), a downstream metabolite of PLA₂, induced by SCI at 24 hours postinjury. (E) AACOCF3 also reversed the decrease of Na⁺, K⁺-adenosine triphosphatase (ATPase) activity at 24 hours after SCI. (F) AACOCF3 resulted in a decrease of myeloperoxidase (MPO) activity at 24 hours postinjury. *p < 0.05, **p < 0.01 versus sham; #p < 0.05, ##p < 0.01 versus vehicle-treated SCI (1-way analysis of variance, Tukey post hoc test); error bars represent mean ± standard error of the mean.