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. 2020 Oct 14;10:17193. doi: 10.1038/s41598-020-74372-7

Figure 2.

Figure 2

TDAG8 deficiency exacerbated the tMCAO-induced cerebral infarction, whereas no appreciable effect was observed by the deficiency of either OGR1 or GPR4. (a-c) Cell damage scores were obtained through analyses of histological Sects. 24 h after the tMCAO/reperfusion. The infarction by the tMCAO in mice deficient in TDAG8 (a), OGR1 (b), and GPR4 (c). Data are shown as the mean ± SEM of each group of WT mice (n = 8 ) and TDAG8-deficient mice (TDAG8Tp/Tp, n = 9), WT mice (n = 9) and OGR1-deficient mice (OGR1−/−, n = 9), and WT mice (n = 10) and GPR4-deficient mice (GPR4−/−, n = 10). Comparisons among groups were assessed using the unpaired Student’s t-test. The effect of TDAG8 deficiency was significant (p < 0.01). No significant difference was observed between WT and OGR1−/− mice or WT and GPR4−/− mice.