硫氧还蛋白还原酶 TrxR2在颅脑损伤大鼠皮质的表达变化

目的：探究硫氧还蛋白还原酶2（TrxR2）在颅脑损伤大鼠皮质的动态表达变化。方法54只雄性 SD 大鼠,随机分为正常对照组（n =6）和颅脑损伤组（n =48）。颅脑损伤组采用改良的 Freeny＆#39;s 自由落体装置制作颅脑损伤大鼠模型,正常对照组不做处理。伤后1 h、3 h、6 h、12 h、24 h、3 d、7 d、14 d,采用实时荧光定量 PCR （quantitative real-time PCR,qRT-PCR）和Western blot 检测挫伤区周围皮质 TrxR2 mRNA 和蛋白的表达变化情况。结果 qRT-PCR 结果显示：皮质中 TrxR2 mRNA 颅脑损伤后1 h 表达增加,24 h 达到高峰,7 d 恢复正常；颅脑损伤组伤后1 h~3 d 各时间点 TrxR2 mRNA 表达明显高于正常对照组（均 P ＜0.05）。Western blot 检测显示：TrxR2蛋白在颅脑损伤后1 h 表达增加,24 h 达到高峰,14 d 恢复正常；颅脑损伤组1 h~7 d 各时间点 TrxR2蛋白表达高于正常对照组（均 P ＜0.05）。结论颅脑损伤后 TrxR2表达增多,提示 TrxR2作为一种急性应激反应蛋白参与颅脑损伤早期抗氧化应激反应。

Expression changes of thioredoxin reductase 2 in rat brain cortex after traumatic brain injury

Objective To investigate the dynamic expression changes of thioredoxin reductase 2 （TrxR2） in rat brain cortex after traumatic brain injury （TBI）. Methods Fifty-four Sprague Dawley male rats were randomly divided into normal control group （n = 6） and TBI group （n = 48）. The TBI model was established in TBI group by the modified Freeny＆#39;s freely falling equipment and no injury was performed in normal control group. Expressions of TrxR2 mRNA and protein were detected in the brain cortex around the contusion area by quantitative real-time PCR （qRT-PCR） and Western blot 1, 3, 6, 12, 24 h, and 3, 7, 14 d after injury. Results qRT-PCR results showed that the expression of TrxR2 mRNA in the brain cortex increased at 1 h, reached peak at 24 h and decreased to normal 7 d after injury in TBI group. Compared with normal control group, the expression of TrxR2 mRNA was significantly higher from 1 h to 3 d after injury in TBI group （all P 〈 0.05）. Western blot results showed that the expression of TrxR2 protein in the brain cortex increased at 1 h, reached peak at 24 h and decreased to normal 14 d after injury in TBI group. Compared with normal control group, the expression of TrxR2 protein was significantly higher from 1 h to 7 d after injury in TBI group （all P 〈 0.05）. Conclusion The expression of TrxR2 in the brain cortex increases after TBI, indicating that TrxR2 may participate in the anti-oxidative stress in the early stage of TBI as an acute stress response protein.