Fig. 7: GPR30 deficiency protects against ischaemia-reperfusion injury after transient middle cerebral artery occlusion.
From: Bicarbonate signalling via G protein-coupled receptor regulates ischaemia-reperfusion injury
a Experimental design of a transient middle cerebral artery occlusion (MCAO) model. b Modified Neurological Severity Score (mNSS) evaluated over time after MCAO. c, d Evaluation of the blood–brain barrier disruption. Representative images (c) and quantification (d) of IgG staining of whole brain sections 3 days after MCAO. Scale bars, 1 mm. e, f Evaluation of infarct volume. Representative images (e) and quantification (f) of cresyl violet staining of whole brain sections 3 days after MCAO. Scale bars, 1 mm. g, h Evaluation of apoptosis using TUNEL staining of whole brain sections 3 days after MCAO. Representative images (g) and quantification (h) of hemibrain sections 3 days after MCAO. The ratio of TUNEL-positive nuclei to total nuclei was calculated on hemibrain sections. TUNEL-positive apoptotic cells were scarcely detectable in GPR30-deficient (Gpr30Venus/Venus) mice. Scale bars, 50 µm. Statistical analysis: b two-tailed mixed-effects analysis with Bonferroni’s multiple comparison correction. Data are presented as the median ± interquartile range. d, f, h two-tailed unpaired t-test. Data are presented as dot plots with the median. P values are shown if significant. ns indicates no significant difference. Source data are provided as a Source Data file.
