Appearance of shortened Bcl-2 and Bax proteins and lack of evidence for apoptosis in rat forebrain after severe experimental traumatic brain injury |
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Authors: | Xiong Y Lin H Chen B D Peterson P L Lee C P |
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Affiliation: | Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA. yexiong@med.wayne.edu |
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Abstract: | To investigate whether apoptosis plays a role in traumatic brain injury (TBI), we examined the expression of Bcl-2 and Bax proteins and the release of mitochondrial cytochrome c in rat brains using Western blot analysis. Bcl-2 at the predicted 26 kDa was not detected in controls and TBI groups. However, at 1 h post-TBI, a shortened Bcl-2 protein with a molecular size of approximately 14.5 kDa was detected in the injured hemisphere (R). At 4 and 12 h post TBI, an additional bcl-2 band ( approximately 10 kDa) was detected in R. Both bands disappeared at 14 days post-injury. The predicted 21-kDa band of Bax was detected in both controls and TBI animals. In addition, two shortened Bax proteins ( approximately 18 kDa) were detected after TBI. The time course of appearance was similar to that of Bcl-2 described above. In the present study, neither cytochrome c release from mitochondria nor DNA fragmentation was detected in the forebrains of sham and TBI groups. Treatment of animals with an antioxidant N-acetylcysteine administered ip greatly diminished the levels of shortened Bcl-2 and Bax proteins. These findings suggest that the induction of shortened Bcl-2 and Bax proteins in rat brains may be associated with reactive oxygen species generated after TBI. |
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