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

Treatment with H2S inhibited TBI-induced oxidative stress and HO-1 expression. (A) The level of MDA in TBI-challenged rats after treatment with NaHS. (B, C) The activities of SOD (B) and GPx (C) in TBI-challenged rats after treatment with NaHS. (D) The mRNA level of HO-1 in TBI-challenged rats after treatment with NaHS. (E) The protein level of HO-1 in TBI-challenged rats after treatment with NaHS. (F) The band density of HO-1 was analyzed using Image J. * P

Figure 4. Treatment with H2S inhibited TBI-induced oxidative stress and HO-1 expression. (A) The level of MDA in TBI-challenged rats after treatment with NaHS. (B, C) The activities of SOD (B) and GPx (C) in TBI-challenged rats after treatment with NaHS. (D) The mRNA level of HO-1 in TBI-challenged rats after treatment with NaHS. (E) The protein level of HO-1 in TBI-challenged rats after treatment with NaHS. (F) The band density of HO-1 was analyzed using Image J. * P<0.05, vs. TBI and TBI+ vehicle groups. #P<0.05, ##P<0.01 vs. sham group.