摘要
目的初步探讨Nrf2-ARE通路在外伤性脑损伤保护作用的机制。方法采用基因敲除大鼠制作创伤性脑损伤模型。将72只实验大鼠分为假手术组(Nrf2+/+)、脑损伤组(Nrf2+/+)、假手术组(Nrf2-/-)和脑损伤组(Nrf2-/-),每组18只。损伤36 h后,采用TUNEL法检测神经细胞凋亡及ELISA蛋白羰基试剂盒检测蛋白质氧化损伤程度。结果假手术组(Nrf2+/+)大鼠与假手术组(Nrf2-/-)大鼠相比,脑组织蛋白羰基浓度及神经细胞凋亡率均无显著差异(P>0.05);而脑损伤组(Nrf2+/+)大鼠及脑损伤组(Nrf2-/-)大鼠的脑组织蛋白羰基浓度及神经细胞凋亡率分别比假手术组(Nrf2+/+)大鼠与假手术组(Nrf2-/-)大鼠高,差异有统计学意义(P<0.01),但脑损伤组(Nrf2-/-)大鼠的相关指标较脑损伤组(Nrf2+/+)明显增高,差异有统计学意义(P<0.01)。结论 Nrf2-ARE通路可能通过减低外伤性脑损伤中脑组织蛋白羰基的浓度,减少神经细胞的凋亡,从而发挥神经保护作用。
Objective To investigate the protective role of Nrf2-ARE signaling pathway in modulating traumatic brain injury （TBI）. Methods Controlled cortical impact （CCI） injury model was performed in Nrf2-knockout or control rats. The 72 rats were randomly divided into four groups consisted of sham Nrf2＋/＋, injured Nrf2＋/＋, sham Nrf2-/- and injured Nrf2-/-, with 18 rats in each group. After 36 h following injury model, TUNEL staining was used to detect neuron apoptosis and ELISA was respectively used to detect levels of oxidation-mediated changes in injury tissue. Results Compared between sham Nrf2~~ group and sham Nrf2^- group the levels of protein carbonyls and the ratio of neuro- cytes apoptosis in injury tissue were no difference （P 〉 0.05）, otherwise compared with rats of sham Nrf2＋/＋group and sham Nrf2-/- group, the levels of protein carbonyls and the ratio of neurocytes apoptosis in injured Nrf2＋/＋ group and injured Nrf2-/- group were significantly decreased （P 〈 0.01）, but compared with rats of injured Nrf2＋/＋ group, these parameters was significantly increased in injured Nrf2- /-group （P 〈 0.01）. Conclusion Nrf2-ARE signaling pathway is probably through to down-regulating the levels of protein carbonyls in injury tissue, decreasing neural cell apoptosis and then provide protection of neurocytes.
出处
《中国现代医生》
2013年第11期11-13,共3页
China Modern Doctor
