Figure 1: Inhibition of S1PR2 results in less oedema and neuronal injury in experimental stroke.
Ischaemia (90 min.) was induced in wild-type (S1pr2+/+) and S1pr2−/− by MCAO. After reperfusion, mice received vehicle or the S1PR2 antagonist, JTE013 (30 mg kg−1), by gavage. (a) Representative images of TTC staining of seven, 1-mm-thick brain coronal slices 24 h after reperfusion. Scale bar, 5 mm. (b) Oedema and (c) infarct ratios were calculated by image analysis and reported as a ratio of the non-ischaemic hemisphere. Infarct ratios were corrected for oedema. The individual values and the mean±s.e.m. are shown. N=10–13 from eight independent experiments. *P<0.05 (one-way ANOVA followed by Newman–Keuls). (d) Improved neurological scores (that is, lower neurological deficit scores) were observed in S1pr2−/− or JTE013-treated S1pr2+/+ mice compared with vehicle-treated S1pr2+/+, 24 h after reperfusion. (e) Representative pictures of TUNEL assay (red channel) in the damaged area from S1pr2+/+, S1pr2−/− and JTE013-treated S1pr2+/+ mice. Blue channel: nuclear staining (DAPI). (f) Quantification of TUNEL-positive cells per mm2. Values are the average of TUNEL-positive cells from three fields. n=4–8 from four independent experiments. Scale bar, 50 μm. (g) Image showing the anatomical areas in which TUNEL-positive cells were quantified in mice (bregma +1.2 to +0.8 mm, rostrally). Scale bar, 2.5 mm.
