摘要
目的探讨纳洛酮对严重颅脑损伤后神经细胞凋亡及Bcl-2、Bax基因表达的影响及其可能的作用机制。方法采用改进的Feeney自由落体损伤模型,应用分子生物学方法-脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(terminal-deoxynucleotidyltransferasemediatednickendlabeling,TUNEL)以及免疫组织化学方法,对严重颅脑损伤大鼠进行纳洛酮治疗,检测受损脑组织中的凋亡细胞和Bcl-2、Bax免疫反应阳性细胞的数量。结果治疗组大鼠脑组织中凋亡细胞数低于损伤对照组,治疗组与损伤对照组之间Bcl-2的表达无显著差异,但治疗组3d、5d组Bax表达明显低于损伤对照组(P<0.05)。结论纳洛酮通过竞争性拮抗内源性阿片肽受体,可能通过抑制Bax的表达来减少颅脑损伤后神经细胞的凋亡,发挥脑保护作用,其详细机理尚有待进一步研究。
Objective To discuss the effect and possible mechanism of naloxone on apoptosis of neuron and expression of Bcl-2 Bax gene after severe brain injury. Methods Severe brain injury rats were treated with naloxone. TUNEL(terminal-deoxynucleotidyl transferase mediated nick end labeling)and immunohistochemisty were used to detect apoptosis and Bcl-2?Bax expression in all the brain tissue. Results The number of TUNEL positive cells in treated group is less than that of control group. There were no significant differences between two groups with Bcl-2 positive cells. While the Bax positive cells in 3d, 5d groups of treated group were obviously less than the controls. Conclusion Naloxone maybe reduce the apoptosis of neuron after brain injury through the inhibiting express of Bax. But its detailed mechanism is still in need for further research.
出处
《中华神经外科杂志》
CSCD
北大核心
2004年第2期170-172,共3页
Chinese Journal of Neurosurgery
