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高梦颖,何永昌,孙国柱,徐伟,武利伟.大鼠液压冲击脑损伤Nrf2、HO-1和NQO-1动态表达变化及意义[J].陆军军医大学学报(原第三军医大学学报),2016,38(18):2023-2028.
Gao Mengying,He Yongchang,Sun Guozhu,Xu Wei,Wu Liwei.Expression of Nrf2, NO-1 and NQO-1 in rat brain following fluid percussion injury[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(18):2023-2028.
高梦颖,何永昌,孙国柱,徐伟,武利伟.大鼠液压冲击脑损伤Nrf2、HO-1和NQO-1动态表达变化及意义[J].陆军军医大学学报(原第三军医大学学报),2016,38(18):2023-2028. DOI:
Gao Mengying,He Yongchang,Sun Guozhu,Xu Wei,Wu Liwei.Expression of Nrf2, NO-1 and NQO-1 in rat brain following fluid percussion injury[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(18):2023-2028. DOI:
目的 探讨大鼠液压冲击伤后水肿脑组织核因子2相关因子2(nuclear factor erythroid-2-related factor 2,Nrf2)、血红素氧化酶-1(heme oxygenase-1,HO-1)和磷酸酰胺腺嘌呤二核苷酸醌氧化还原酶-1 (NADPH quinineoxidoreductase-1,NQO-1)的表达变化及其意义。 方法 成年雄性SD大鼠56只制作液压冲击颅脑损伤模型,术后1 h、6 h、12 h、24 h、3 d、7 d用干湿质量法测定脑组织含水量,Western blot测定Nrf2胞浆、胞核蛋白以及HO-1、NQO-1蛋白;用实时荧光定量PCR测定Nrf2 mRNA表达。 结果 自冲击伤后6 h,脑组织含水量开始增加,24h达高峰,持续至3 d,然后开始下降(P0.05)。组织学观察印证了脑水肿趋势。Western blot检测结果显示胞浆Nrf2蛋白于伤后12 h开始持续降低,而胞核Nrf2蛋白则于1h开始升高,24 h达到高峰,3 d时降低,7 d后明显降低,但仍高于NC组(P0.05)。HO-1和NQO-1蛋白表达与胞核Nrf2蛋白趋势一致。实时荧光定量PCR显示TBI组术后各时间点Nrf2 mRNA表达水平无明显变化(P0.05)。 结论 液压冲击伤后出现核因子Nrf2转位激活,可能通过上调HO-1、NQO-1蛋白表达发挥神经保护作用。
Objective To investigate the expression alternation of nuclear factor erythroid 2-related factor 2 (Nrf2)
hemeoxygenase-1 (HO-1) and NADPH:quinine oxidoreductase (NQO-1) in rats following fluid percussion injury. Methods Traumatic brain injury (TBI) model in rats was established by fluid percussion injury (n=56). At 1
6
12 and 24 h
and 3 and 7 d after operation
the water content in brain tissues was quantified by dry-wet measurement
and the protein expression levels of Nrf2 (cytoplasm and nuclear)
NO-1 and NQO-1 were detected by Western blotting. Also
the mRNA expression of Nrf2 was measured by real-time (RT) PCR. Results Comparing with normal control (NC) group
the water content in TBI group increased after 6 h
reaching the peak at 24 h and retaining for 3 d
and then dropped (P0.05). This was in agreement with the edema tendency in injured brain tissue observed by pathohistological staining. Moreover
Western blotting result showed the same change trend in protein expression of Nrf2 in nuclei
NO-1 and NQO-1 but not Nrf2 in cytoplasm. Only after 7 d
their expression was remarkably decreased but still higher than NC group (P0.05). The expression of Nrf2 in cytoplasm was consistently decreased after 12h of the injury. In addition
RT-PCR analysis showed that there were no significant differences in Nrf2 mRNA levels in TBI group at different time points (P0.05). Conclusion Nrf2 is translocated and activated in rats following fluid percussion injury
indicating that Nrf2-ARE signaling pathway may be involved in neuro-protection via upregulating expression of NO-1 and NQO-1 proteins in TBI.
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