Résumé
<p><b>OBJECTIVE</b>Some 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.</p><p><b>METHODS</b>Ninety 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.</p><p><b>RESULTS</b>The 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).</p><p><b>CONCLUSIONS</b>The 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.</p>