目的:观察过表达B细胞淋巴瘤/白血病-2(bcl-2)对重度创伤性脑损伤大鼠神经保护作用。方法:2018年1月至2019年9月，60只SD大鼠采用随机数字法分为对照组、模型组和bcl-2组。对照组和模型组大鼠经脑室注射对照腺相关病毒1×10n 11 v.g/只，bcl-2组经脑室注射bcl-2过表达腺相关病毒1×10n 11 v.g/只，注射24 d后，模型组和bcl-2组大鼠采用自由落体撞击法建立重度创伤性脑损伤模型，对照组大鼠不处理。建模24 h后，采用神经行为学评分评价大鼠的神经功能；采用原位缺口末端标记法(TUNEL)染色分析脑组织的凋亡水平；采用JQ1法检测脑组织细胞线粒体膜电位；采用蛋白质印迹法(Western blot)分析bcl-2、bcl-2相关X蛋白(bax)和半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3蛋白表达水平，计量资料比较采用单因素方差分析。n 结果:bcl-2组大鼠神经功能评分(5.72±1.27)低于模型组大鼠神经功能评分(8.59±1.67)，差异有统计学意义(n t＝3.114，n P<0.05)。bcl-2组大鼠脑组织细胞线粒体膜电位(1.59±0.13)高于模型组大鼠脑组织细胞线粒体膜电位(1.01±0.10)，差异有统计学意义(n t＝2.011，n P<0.05)。bcl-2组大鼠神经细胞凋亡水平[(16.59±3.09)%]显著低于模型组[(39.54±4.09)%]，差异有统计学意义(n t＝3.103，n P<0.05)。bcl-2组细胞bcl-2蛋白表达水平(1.79±0.14)高于对照组和模型组(0.96±0.11和1.00±0.12)，差异有统计学意义(n t＝2.019、1.978，n P<0.05)。bcl-2组大鼠脑组织Caspase-3和bax蛋白表达水平(1.17±0.09和1.05±0.17)低于模型组(1.32±0.11和1.74±0.12)，差异有统计学意义(n t＝1.280、2.016，n P<0.05)。n 结论:过表达bcl-2可显著抑制重度创伤性脑损伤大鼠神经细胞凋亡，提高线粒体功能，保护大鼠神经功能。“,”Objective:To investigate the neuroprotective effect of overexpression of B cell lymphoma/leukemia-2 (bcl-2) on rats with severe traumatic brain injury.Methods:From January 2018 to September 2019, a total of 60 SD rats were purchased from Shanghai SLAC Laboratory Animal Co., Ltd and randomly divided into control group, model group and bcl-2 group. Rats in control group and model group were intraventricularly injected with 1×10n 11 v. g control adeno-associated virus, and those in bcl-2 group were injected with 1×10n 11 v. g bcl-2. After 24 days of injection, severe traumatic brain injury model was established in model group and bcl-2 group by free falling impact method, while the animals in control group were not treated. At 24 h after modeling, the neurological function of rats was evaluated by neurobehavioral score. The apoptosis level of brain tissue was analyzed by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The mitochondrial membrane potential of brain tissue was detected by JC-1 method. The protein expression levels of bcl-2, bcl-2 associated X protein (bax) and cysteinyl aspartate specific proteinase-3 (Caspase-3) were analyzed by Western blotting. One-way analysis of variance (ANOVA) was used to compare the data between groups.n Results:Compared with the model group (8.59±1.67), the neurological function score in bcl-2 group was significantly decreased (5.72±1.27, n t=3.114, n P<0.05). Compared with the model group (1.01±0.10), the mitochondrial membrane potential (1.59±0.13) in bcl-2 group was significantly increased (n t=2.011, n P<0.05). Compared with the model group [(39.54±4.09)%], the apoptosis level in bcl-2 group [(16.59±3.09)%] was significantly decreased (n t=3.103, n P<0.05). Compared with control group and model group [(0.96±0.11) and (1.00±0.12)], the expression level of bcl-2 protein in bcl-2 group was significantly increased (1.79±0.14,n t=2.019, 1.978, n P<0.05). Compared with the expression levels of bax and Caspase-3 protein in the model group (1.32±0.11, 1.74±0.12), the expression levels of Caspase-3 and bax proteins in brain tissue of bcl-2 group (1.17±0.09, 1.05±0.17) were significantly decreased (n t=1.280, 2.016, n P<0.05).n Conclusion:Overexpression of bcl-2 can significantly inhibit neuronal apoptosis, improve mitochondrial function and protect neural function in rats with severe traumatic brain injury.