大鼠液压脑损伤后Bcl-2、Bcl-x和Bax蛋白表达的改变

目的：探讨液压脑损伤后凋亡相关基因bcl-2、bcl-x和bax在蛋白水平的表达变化规律及神经细胞凋亡的分子生物学机制。方法：应用免疫组化方法分别检测大鼠中型液压脑损伤后不同时程Bcl-2、Bcl-x和Bax蛋白表达情况。结果：伤后6h,打击侧海马CA3区bcl-2和Bcl-x蛋白表达显著下降，Bax的表达无明显变化，(Bcl-2 Bel-x)/Bax比率下降主要由于前者下降所致。伤后1-3d,Bax蛋白表达显著增加，Bcl-2和Bcl-x的表达下降相对缓慢，（Bcl-2 Bcl-x)/Bax比率同样减小。结论：bcl-2基因家族参与了液压脑损伤后神经细胞凋亡，该基因家族不同成员的表达变化与神经细胞凋亡有关。

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

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.