Cell apoptosis and Bcl-2 gene therapy following traumatic brain injury

Objective To study the cell apoptosis following traumatic brain injury （TBI） and explore the therapeutic effect of Bcl-2 gene therapy on it. Methods A total of 60 SD rats were assigned randomly to TBI group （ n = 15 ）, sham control group （ n = 15 ） ,gene therapy group （ n = 15 ） and Empty- Vec control group （ n = 15 ）. Except for sham control group, rats were subjected to severe TBI by Feeney＇ s method. The cDNA of Bcl-2 gene was cloned by RT-PCR. A recombinant eukaryotic expression vector was constructed to transfect the injured brain cells and Bcl-2 expression in vivo was detected by immunofluorescence. The cell apoptosis of each group was detected by TUNEL and electron microscopy. Results Compared with sham control group, more apoptotic cells were found around the traumatic focus in TBI group, with a significant statistical difference in the apoptosis index between two groups （P 〈 0.01 ）. Bcl-2 was expressed successfully in vivo after lipofection. The Bcl-2 （ ＋ ） cell labeling index was （8.3 ＋ 0.7） % in gene therapy group and only （0.9 ＋ 0. 2 ） % in Empty-Vec group （ P 〈 0. 01 ）, which suggested that enhanced expression of Bcl-2 resulted in a decline in apoptosis. Conclusions It is found in the present study that apoptosis occurs following TBI. Bcl-2 expression in vivo can inhibit apoptosis, which provides a practicable way for early intervention to promote cell survival. Key words: Brain injuries, traumatic;  Genes, Bcl-2;  Gene therapy;  Apoptosis