Exogenous S1P Exposure Potentiates Ischemic Stroke Damage That Is Reduced Possibly by Inhibiting S1P Receptor Signaling

Figure 7

Activation of S1P signaling induces augmented TNF-α expression following M/R injury. S1P or vehicle (veh) was injected into the corpus callosum 24 h prior to M/R challenge (60 min occlusion followed by 22 h reperfusion). FTY720 (FTY) was administered into mice 30 min prior to S1P microinjection (FTY + S1P) or 60 min occlusion (S1P + FTY + M/R). Cells expressing TNF-α were assessed 1 day or 22 h after S1P microinjection or reperfusion. Representative microphotographs of brain sections immunolabeled against TNF-α (a) and their quantitative analysis (b) in groups of sham, S1P, FTY + S1P, veh + M/R, S1P + M/R, and S1P + FTY + M/R. Significance was presented only for the main groups as indicated. , compared with M/R group (veh + M/R) (Newman-Keuls test). , compared with the S1P or S1P + M/R group (Newman-Keuls test). per group. Scale bar, 50 µm.

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