摘要
目的:探讨二甲胺四环素(minocycline)对大鼠脊髓损伤后神经细胞凋亡和相关因子表达的影响及对损伤脊髓神经功能的保护作用。方法:36只SD大鼠分为4组,空白组只暴露脊髓,不损伤,A、B组及损伤组建立脊髓损伤模型。A、B组分别给予二甲胺四环素和甲基强的松龙腹腔内注射;损伤组和空白组腹腔内注射生理盐水。免疫组化法检测4组大鼠损伤脊髓神经细胞凋亡因子(Bcl-2、Bcl-xl、Bax)的表达;TUNEL标记凋亡细胞。结果:A组的神经功能高于损伤组(P<0.01),与B组差异无显著性意义;损伤组的凋亡阳性细胞多于A、B组(P<0.05);A组Bcl-2阳性表达细胞多于损伤组(P<0.05),而Bcl-xl、Bax表达与损伤组差异无显著性意义。结论:凋亡是脊髓损伤后神经细胞死亡的一种重要方式;二甲胺四环素能上调Bcl-2的表达,改变Bcl-2/Bax的比值,从而抑制脊髓神经细胞凋亡,对损伤脊髓的神经功能有保护作用。
Objective： To observe the expression of apoptosis factors, the mechanism of neuronal apoptosis and protective effect of minocycline after spinal cord injury （SCI） in rats. Methods： Thirty-six SD rats were divided into 4 groups： control group, injury group, treatment groups A and B. The animal SCI model was established by Allen＇s method. The changes of nerve functions of rats in 4 groups were observed after treatment with minocycline or methylprednisolone. The expressions of apoptosis factors （Bcl-2, Bax, Bcl-xl） was detected by immunocytochemistry technique, and apoptosis neurons were labeled with TUNEL dyeing. Results： The grade of nerve function was improved distinctly in treatment groups （P^0. 05）, but there was no significant difference between treatment groups. The number of the positive cells for bcl-2 in treatment group.s was more than that in injury group （P~ 0.05）, but there was no significant difference in the expression of Bax and Bcl-xl between injury group and minocycline treatment group. Conclusion： Apoptosis is an important death mode of neuron after SCI; Minocycline can upregulate bcl-2, distinctly improve the comeback of the nerve function and protect the nerve tissue.
出处
《中国康复》
2005年第5期259-261,共3页
Chinese Journal of Rehabilitation
