The expression and effect of IL-18 after hypoxic-ischemic brain damage

Objective To explore the expression and effect of interleukin(IL)-18 after hypoxic-ischemic brain damage(HIBD) in neonatal rats. Methods The HIBD model of seven-day-old Wistar rats was established. The mRNA and protein for IL-18 in cerebral cortex of control group, HIBD3 h, 8 h, 24 h, 3 d, 6 d and 14 d group were analyzed by RT-PCR and immunohistochemistry respectively, at the same time histological changes were observed. Results The expression of IL-18 mRNA and protein was low in control group[mRNA: 0.321 8±0.046 6; protein: (6.033± 1.019)cells/field]. After HIBD, the level of mRNA/protein for IL-18 in ischemic cortex increased progressively at 24 h to 6 d [mRNA: 24 h: 0.582 3±0.074 0, 3 d:0.697 6 ±0.107 3, 6 d: 0.911 0±0.064 7; protein: 24 h: (19.133±2.094)cells/field, 3 d: (28.900 ±1.589) cells/field, 6 d: (52.883±3.203)cells/field; P0.01 vs control], and reached its greatest level at 6 d (P0.01 vs other groups). The mRNA/protein for IL-18 decreased significantly at 14 d of reperfusion[mRNA: 0.579 3±0.084 2; protein:(16.767±2.381)cells/field], but was still higher than the normal level(P 0.01 vs control). Histological study showed that the degenerated and necrotic neurons increased progressively at 1 d to 6 d after HIBD, at the same time the proliferation of glial cells appeared. Conclusion The increasing expression of IL-18 mRNA/protein after HIBD was delayed and lasting, which implied that it may play an important role in late-stage inflammatory responses to HIBD in neonatal rats.