Research Paper Volume 13, Issue 5 pp 7180—7189

Neuroprotective effect of hydrogen sulfide against glutamate-induced oxidative stress is mediated via the p53/glutaminase 2 pathway after traumatic brain injury

p53 inhibition reversed the effect of H2S on glutamate and glutamate-mediated oxidative stress after TBI. (A) The protein level of GLS-2 and p53 in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (B, C) The band density of GLS-2 (B) and p53 (C) was analyzed using Image J. (D) The level of glutamate in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (E) The level of MDA in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (F, G) The activities of SOD (F) and GPx (G) in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. * P

Figure 5. p53 inhibition reversed the effect of H2S on glutamate and glutamate-mediated oxidative stress after TBI. (A) The protein level of GLS-2 and p53 in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (B, C) The band density of GLS-2 (B) and p53 (C) was analyzed using Image J. (D) The level of glutamate in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (E) The level of MDA in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. (F, G) The activities of SOD (F) and GPx (G) in TBI-challenged rats after co-treatment with NaHS and pifithrin-α. * P<0.05, vs. TBI+NaHS+ pifithrin-α group. #P<0.05, vs. TBI+ vehicle group. @P<0.05, @@<0.01, vs. sham group.