OBJECTIVESome research has shown that the brain white matter damage is closely related to apoptosis of pre-oligodendrocytes. The relationship of bcl-2 protein, a protein of anti-apoptosis, with brain white matter damage in neonatal rats is rarely reported. This study examined the changes of bcl-2 protein expression following brain white matter damage in neonatal rats.

METHODSNinety 2-day-old Sprague-Dawley (SD) rats were randomly divided into 2 groups: experimental group (n=45) and control group (n=45). Brain white matter damage was induced by ligation of the right common artery, followed by 6% hypoxia exposure in the rats from the experimental group. The rats of the control group were sham-operated, without hypoxia-ischemia treatment. The expression of bcl-2 protein in the periventricular white matter and the callositas was detected by immunohistochemical technique. Apoptosis of neurocytes in these tissues was detected by TUNEL.

RESULTSThe apoptosis index of neurocytes in the experimental group was up-regulated at 4, 12 and 24 hrs and at 3 and 7 days, peaking at 3 days after white matter damage, compared with the control group (P < 0.05). The expression of bcl-2 protein in the experimental group began to increase at 1 hr, reached a peak at 12 hrs and remained a higher level until 3 days after white matter damage compared with that observed in the control group (P < 0.05).

CONCLUSIONSThe expression of bcl-2 protein increased at the early stage of white matter damage in neonatal rats. The peak of apoptosis lagged behind that of the bcl-2 protein expression, which suggests that bcl-2 protein may have protective effects against neuronal apoptosis.