Role of inflammation and free radical in nerve cell apoptosis in newborn rats with hypoxic-ischemic brain damage / 中华实用儿科临床杂志

Objective To explore the changes of tumor necrosis factor-α (TNF-α),nuclear factor kappa B (NF-κB),free radical in brain tissue in newborn rats with hypoxic-ischemic brain damage(HIBD),to clarify the role of TNF-α,NF-κB,free radical in HIBD.Methods The 56 SD neonatal rats were randomly divided into control group and hypoxic-ischemic 6 h,12 h,24 h,48 h,72 h,7 d groups.The conventional method was used to establish HIBD model.The level of TNF-α was measured by enzyme-linked immumosorbent assay,NF-κB was detected by electrophoretic mobility shift assay.The neuron apoptosis was identified by flow cytometry.Superoxide dismutase(SOD),molondialdehyde (MDA),glutathione peroxidase(GSH-Px) were identified by spectrophotography.Results The rate of neuron apoptosis,the contents of TNF-α,NF-κB,MDA in brain tissue were significantly higher in 6 h,12 h,24 h,48 h,72 h groups than those in contral group(all P ＜0.05),and the apoptosis,MDA reached the peak at the 24 h after hypoxia,TNF-α reached the peak at the 12 h after hypoxia,NF-κB reached the peak at the 48 h after hypoxia.But the content of SOD and the activity of GSH-Px in hypoxic-ischemic group were significantly lower than those in control group at 6 h,12 h,24 h,48 h,72 h after hypoxia.And the rate of neuronal apoptosis was positively correlated with TNF-α,NF-κB and MAD (all P ＜ 0.05),negatively correlated with GSH-Px and SOD (all P ＜ 0.05),the contents of TNF-α,NF-κB were positively correlated with MAD (all P ＜ 0.05),negatively correlated with the content of SOD and the activity of GSH-Px (all P ＜ 0.05).Conclusions TNF-α,NF-κB,free radical are early changed after HIBD,So they play an important role in HIBD,inflammation and free radical can promote brain damage.

Relation of inflammatory inhibition and headache after subarachnoid hemorrhage / 中国康复理论与实践

@#ObjectiveTo explore pathogenesis of headache after subarachnoid hemorrhage (SAH) whether related with immune inflammatory reaction in subarachnoid and observe the effect of immunosuppressive action of dexamethasone on headache.Methods80 patients who was consciousness and complained headache after SAH were randomly divided into four groups, treated only with mannitol, mannitol plus cerebrospinal fluid (CSF) replacement, intrathecal and vein injection with dexamethasone. Effects of four groups were observed.ResultsEfficiencies of four groups were respectively the mannitol group 27.27%, the permutation group 66.67%, the intrathecal group 92.36% and the vein group 30.00%. There was a significantly difference between the intrathecal group and other three groups, and the time of headache remission for intrathecal group was also longer than that of other three groups (P<0.01).ConclusionThe wide immune inflammatory responses in subarachnoid induced by degenerative and hemic CSF is likely main cause of headache after SAH and intrathecal injection with dexamethasone has an obviously effect.