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目的研究选择性环氧合酶-2抑制剂——塞来昔布对大鼠颅脑创伤后凋亡蛋白Bcl-2和Bax表达的影响。方法按照体重将SD大鼠随机分为4组:实验组、模型组、假手术组和对照组,实验组和模型组构建大鼠闭合性颅脑创伤模型。在颅脑损伤模型构建后,实验组立即经腹腔注入塞来昔布250mg·kg-1;模型组、假手术组和对照组给于同等量的0.9%Na Cl腹腔注射。用免疫印迹法和免疫组织化学染色法检测凋亡蛋白Bcl-2和Bax的表达。结果实验组、模型组、假手术组和对照组的各组Bcl-2蛋白表达量分别为68.75±0.62,45.40±0.36,81.08±0.65,78.12±0.05,与假手术组和对照组比较,模型组Bcl-2蛋白表达量明显降低,差异有统计学意义(P<0.05);与模型组比较,实验组Bcl-2蛋白表达量明显增加,差异有统计学意义(P<0.05)。实验组、模型组、假手术组和对照组的各组Bax蛋白表达量分别为68.28±0.35,92.48±0.16,65.06±0.63,63.15±0.10,与假手术组和对照组比较,模型组Bax蛋白表达量明显增加,差异有统计学意义(P<0.05);与模型组相比较,实验组Bax蛋白表达量明显降低,差异有统计学意义(P<0.05)。结论塞来昔布可通过增加脑组织Bcl-2的表达、降低Bax的表达和抑制脑损伤后神经细胞的凋亡,对大鼠颅脑创伤具有保护作用。
Objective To investigate the effect of selective cyclooxygenase-2 inhibitor-celecoxib on the expression of Bcl-2 and Bax after traumatic brain injury in rats. Methods According to body weight, SD rats were randomly divided into 4 groups: experimental group, model group, sham operation group and control group. The experimental group and model group were established closed brain injury model. In the model of craniocerebral injury, celecoxib 250 mg · kg-1 was injected into the experimental group immediately. The model group, sham-operation group and control group were injected intraperitoneally with the same amount of 0.9% NaCl. Western blotting and immunohistochemistry were used to detect the expression of Bcl-2 and Bax. Results The expression of Bcl-2 protein in the experimental group, model group, sham operation group and control group were 68.75 ± 0.62, 45.40 ± 0.36, 81.08 ± 0.65, 78.12 ± 0.05, respectively. Compared with the sham group and the control group, Compared with the model group, the expression of Bcl-2 protein in the experimental group was significantly increased, the difference was statistically significant (P <0.05). The expression of Bax in experimental group, model group, sham operation group and control group were 68.28 ± 0.35,92.48 ± 0.16,65.06 ± 0.63,63.15 ± 0.10, respectively. Compared with sham group and control group, Bax protein expression in model group (P <0.05). Compared with the model group, the expression of Bax protein in the experimental group was significantly decreased, the difference was statistically significant (P <0.05). Conclusion Celecoxib can protect the brain from traumatic brain injury in rats by increasing the expression of Bcl-2, decreasing the expression of Bax and inhibiting the apoptosis of neural cells after brain injury.