• Chun Luo, Yicheng Lu, Jiyao Jiang, and Cheng Zhu.
• Department of Neurosurgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. luochun@sh163a.sta.net
• Chin. J. Traumatol. 2002 Oct 1; 5 (5): 299-302.

ObjectiveTo investigate the changes of bcl-2 gene family and the molecular mechanism of neuronal apoptosis following traumatic brain injury (TBI) in rats.MethodsMale Sprague-Dawley (SD) rats were subjected to lateral fluid percussion brain injury (FPBI) of moderate severity. The bcl-x(L) and bax mRNA expression was detected by reverse transcription polymerase chain reaction (RT-PCR). In addition to morphological evidence of apoptosis, terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labeling (TUNEL) histochemistry was used to identify the DNA fragmentation in situ at both light and electron microscope levels, whereas characteristic internucleosomal DNA fragmentation of apoptosis was demonstrated by DNA gel electrophoresis.ResultsThe apoptotic response to trauma was regionally distinct and may be involved in both acute and delayed cell death. The bcl-x(L) mRNA expression of the impact site was significantly lower (67.42%+/-7.54%) than that of the ipsilateral hemisphere at 6 hours after injury (P<0.01). The decrease of bcl-x(L) mRNA expression preceded apoptosis at 24 hours after injury. The bax mRNA expression rose slowly, doubled at 3 days after injury and returned to the sham level slowly.ConclusionsDecreased expression of bcl-x(L) mRNA and increased expression of bax mRNA coincides with apoptosis following brain injury. The bcl-2 gene family is involved in neuronal apoptosis after TBI, and the changes of mRNA expression of the family members lead the neuronal cells to apoptosis.

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