Skip to main content
. 2022 Dec 29;24(1):582. doi: 10.3390/ijms24010582

Figure 1.

Figure 1

αN-acetyl β-End 1–31 reduced ischemic brain damage and diminished seizures induced by NMDAR overactivation. Implication of σ1Rs. (A) αN-acetyl β-End 1–31 administration diminished ischemic brain damage in wild-type but not σ1R−/− mice. Upper panel: representative 2,3,5-triphenyltetrazolium chloride (TTC)-stained brain section images obtained from saline- and drug-treated mice (3 nmol, 1 h after surgery) 48 h after pMCAO. White indicates infarction; red staining indicates normal tissue. Lower panel: the bar graphs quantitatively compare the infarct volume based on TTC staining from wild-type mice treated with saline, β-End 1–31 and the σ1R agonist PRE084 (white bars). The reducing effect of αN-acetyl β-End 1–31 was counteracted by β-End 1–31 and PRE084 (gray bars). In σ1R−/− mice, the positive effect of αN-acetyl β-End 1–31 was not observed. The groups consisted of five to eight mice, and the data are presented as the mean ± SD. * Significantly different from the saline-treated mice. ϕ Significantly different from mice receiving only αN-acetyl β-End 1–31; ANOVA followed by the Holm–Sidak multiple comparisons test, p < 0.05, 1-β > 0.80. (B) Anticonvulsant effects of αN-acetyl β-End 1–31 in a mouse model of seizures induced by NMDAR overactivation. Effects of PPCC, β-End 1–31 and αN-acetyl β-End 1–31 on seizures induced by NMDA in wild-type and σ1R−/− mice. The mice received icv 1 nmol of the NMDAR agonist NMDA 30 min after the other drugs (3 nmol) and were then immediately evaluated. Each bar indicates the percentage of mice showing the indicated sign and represents the mean ± SD of eight mice. * Significant difference from the control group that received NMDA and saline instead of the drugs. ϕ Significant difference from the corresponding NMDA-induced behavioral signs exhibited by the group that received only αN-acetyl β-End 1–31. θ Significant difference from the corresponding NMDA-induced behavioral signs exhibited by the wild-type group that received only αN-acetyl β-End 1–31. ANOVA followed by the Holm–Sidak multiple comparisons test, p < 0.05, 1-β > 0.80.