Role of inflammation and free radical in nerve cell apoptosis in newborn rats with hypoxic-ischemic brain damage

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 mo-bility 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. Key words: hypoxia-ischemia; tumor necrosis factor-α; nuclear factor-kappa B; inflammation; rat, newborn