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Alteration of Bcl-2, Bcl-x and Bax protein expression following fluid percussion brain injury in rats

Yi Lü

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Abstract

Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

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Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

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Available abstract

Objective: To investigate the alteration of bcl 2 gene family in the rat brain and the molecular mechanism of neuronal apoptosis following traumatic brain injury. Methods: Male Sprague Dawley rats were subjected to lateral fluid percussion brain injury(FPI) of moderate severity. Bcl 2, Bcl x and Bax protein expression was detected by immunohistochemistry. Results: (1) The immunoreactivity of Bcl 2 and Bcl x protein decreased in the hippocampus ipsilateral impact site as early as 6 h post injury, and this was the main cause of down regulation of the ratio of Bcl 2+Bcl x to Bax. (2) During 1 3 d after injury, the Bax protein expression increased significantly, while the Bcl 2 and Bcl x protein expression decreased relatively slow. The decreased ratio of Bcl 2+Bcl x to Bax was mainly due to the Bax up regulation. Conclusion: The bcl 2 gene family is involved in neuronal apoptosis after FBI, and the protein expression alteration of the family members leads the neuronal cell to apoptosis.

Key concepts: Apoptosis, BAX Protein, Immunohistochemistry, Hippocampus, Gene, Protein expression, Bcl-2 family, Bcl-2-associated X protein

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