塞来昔布对颅脑创伤后大鼠的凋亡蛋白Bcl-2和Bax表达影响

Effects of celecoxib on expression of apoptosis protein Bcl-2 and Bax after craniocerebral injury in rats

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 effects of celecoxib （selective cyclooxygenase-2 inhibitor） on the expression of Bcl-2 and Bax in rat brain after severe craniocerebral injury in rats. Methods SD rats were randomly divided into four groups：experimental group, model group, sham operation group and control group. The rats in experimental group and model group were established with closed craniocerebral injury model. In the experimental group, intraperitoneal injection of celecoxib （250 mg· kg^-l） was performed immediately after the craniocerebral in- jury model was established. The rats in＇Sham operation group and the control group were given the same amount of 0.9% NaC1 intraperitonea- lly, The expressions of Bcl -2 and Bax mRNA and protein were detected by immunohistochemical staining. Results The expression of Bcl -2 protein in the experimental group, model group, sham - operated group and control group were 68.75 ±0. 62, 45.40 ±0. 36, 81.08± 0. 65, 78.12±0.05. The expression of Bcl -2 in the model group was significantly lower than in sham - operated group and control group with significantly （ P 〈 0.05 ）. Compared with the model group, the expression of Bcl -2 in the experimental group decreased with significantly （P 〈 O. 05 ）. The expression of Bax protein in experimental group, model group, sham operation group and control group respectively were 68.28 ± 0. 35, 92.48 ± 0. 16, 65.06 ± 0. 63, 63.15 ± 0. 10. The expression of Bax in model group was signifi- cantly higher than in sham - operated group and control group with significantly （P 〈 0. 05）. Compared with the model group, the expression of Bax in the experimental group decreased with significandy（P 〈 0. 05 ）. Conclusion Celecoxib can increasing the expression of Bcl - 2, decreasing the expression of Bax, inhibiting the apoptosis of neurons after ranio- cerebral injury, has a protective effect on the traumatic brain injury in rats.