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目的研究缺氧预处理对颅脑损伤大鼠皮层核转录因子NF-E2相关因子2(Nrf2)、血红素加氧酶1(HO-1)表达变化的影响。方法 216只SD雄性大鼠,随机分为对照组(Con)、缺氧预处理组(HP)、颅脑损伤组(TBI)、缺氧预处理+颅脑损伤组(HP+TBI);Con和HP组各12只,TBI和HP+TBI组根据伤后处死时间再分为1 h、3 h、6 h、12 h、24 h、3 d、7 d、14 d八亚组,每组12只。采用改良的Feeney’s自由落体装置制作颅脑损伤大鼠模型,先在低压氧舱内处理3 d(-50 kPa、3 h/d)制作缺氧预处理模型。四组均用免疫组化和Western blotting测定Nrf2、HO-1的表达变化。结果颅脑损伤后皮层Nrf2和HO-1在伤后1 h开始表达升高,24 h达高峰,3 d后下降,1 h~7 d各时间点,TBI与Con组、HP+TBI与HP组相比,差异有统计学意义(P<0.05)。单纯3 d缺氧预处理后HP组与Con组比较,Nrf2、HO-1的表达差异无统计学意义;伤后1 h~7 d,HP+TBI组Nrf2、HO-1表达较TBI组更高,差异有统计学意义(P<0.05)。结论缺氧预处理进一步增加大鼠颅脑损伤后皮层Nrf2、HO-1表达,提高颅脑损伤后脑组织的抗氧化能力。
Objective To investigate the effects of hypoxia preconditioning on the expression of nuclear factor-2 (NF-kappa2) and heme oxygenase-1 (HO-1) in the cortex of rats with craniocerebral injury. Methods Totally 216 SD male rats were randomly divided into control group (Con), hypoxic preconditioning group (HPI), TBI group, hypoxic preconditioning group and HP + TBI group. Con And 12 in HP group. TBI and HP + TBI groups were further divided into eight sub-groups: 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, 7 d and 14 d 12 only. A rat model of traumatic brain injury was established by using a modified Feeney’s free-fall device. The hypoxic preconditioning model was established by treating the injured brain in a hypobaric chamber for 3 days (-50 kPa, 3 h / d). The four groups were detected by immunohistochemistry and Western blotting Nrf2, HO-1 expression changes. Results The expression of Nrf2 and HO-1 in the cortex at 1 hour after TBI increased significantly, reached the peak at 24 hours, decreased at 3 days and decreased at 1 h to 7 d Group, the difference was statistically significant (P <0.05). Compared with Con group, the expression of Nrf2 and HO-1 had no significant difference after 3 days hypoxia preconditioning, while the expression of Nrf2 and HO-1 in HP + TBI group was more than that in TBI group at 1 h to 7 d High, the difference was statistically significant (P <0.05). Conclusions Hypoxic preconditioning can further increase the expression of Nrf2 and HO-1 in the cortex after traumatic brain injury in rats, and improve the anti-oxidative ability of brain tissue after traumatic brain injury.