Regular Article
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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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 ∼14.5 kDa was detected in the injured hemisphere (R). At 4 and 12 h post TBI, an additional bcl-2 band (∼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 (∼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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    1

    To whom correspondence should be addressed at Department of Biochemistry and Molecular Biology, School of Medicine, Wayne State University, 540 East Canfield Street, Detroit, MI 48201. Fax: (313) 577-1158. E-mail: [email protected].

    2

    Current address: Department of Neurology, Dickinson Medical Building, 1711 South Stephenson Avenue, Iron Mountain, MI 49801.

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