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目的探讨Caspase-12参与高氧所致新生小鼠胼胝体白质损伤的情况。方法新生6天的C57BL/6小鼠共12组,随机分为高氧组及对照组。高氧组分别给予高氧24 h或48 h以及高氧48 h后在小鼠日龄的10、12、15、30天(P10、P12、P15、P30)断头取脑,并与相应日龄对照组进行对比。检测不同日龄小鼠胼胝体白质髓鞘碱性蛋白(MBP)表达,检测高氧24、48 h后小鼠胼胝体白质Caspase-12 mRNA及蛋白表达,TUNEL法检测小鼠胼胝体白质细胞凋亡。结果 P10、P12高氧组MBP表达水平低于对照组,差异有统计学意义(P=0.004,0.016);P15、P30两组比较,差异均无统计学意义(P>0.05)。高氧24、48 h后与对照组24、48 h比较,Caspase-12 mRNA相对表达量分别为(1.549±0.098)比(1.080±0.101)和(1.333±0.076)比(1.022±0.089),cleavedCaspase-12蛋白相对表达量分别为(1.582±0.010)比(0.994±0.078)和(1.370±0.095)比(0.978±0.069),高氧组均高于其对照组,差异有统计学意义(P<0.05)。高氧24、48 h与对照组相比,Caspase-12抗原表达阳性细胞显著增加。P10、P12高氧组凋亡指数高于对照组(18.742±2.503比4.587±2.353,36.184±3.655比5.351±2.678),差异有统计学意义(P<0.05)。结论高氧暴露可导致新生小鼠胼胝体白质损伤,可能通过提高Caspase-12表达使胼胝体白质细胞过度凋亡,进而导致胼胝体白质损伤。
Objective To investigate the role of Caspase-12 in the corpus callosum white matter injury induced by hyperoxia. Methods Twelve newborn C57BL / 6 mice were randomly divided into hyperoxia group and control group. The rats in hyperoxia group were exposed to hyperoxia for 24 h or 48 h, respectively. After 48 h of hyperoxia exposure, brains were decapitated at days 10, 12, 15 and 30 (P10, P12, P15 and P30) Age control group for comparison. The expression of myelin basic protein (MBP) in corpus callosum of different age mice was detected. The mRNA and protein expression of Caspase-12 in corpus callosum were detected at 24 and 48 h after hyperoxia. The apoptosis of corpus callosum was detected by TUNEL. Results The expression of MBP in P10 and P12 hyperoxia group was lower than that in control group (P = 0.004,0.016). There was no significant difference in P15 and P30 between the two groups (P> 0.05). The relative expression levels of Caspase-12 mRNA in 24 h and 48 h after hyperoxia were (1.549 ± 0.098) vs (1.080 ± 0.101) and (1.333 ± 0.076), respectively (1.022 ± 0.089), cleaved Caspase (1.582 ± 0.010) vs (1.370 ± 0.095) vs (0.978 ± 0.095), respectively, in hyperoxia group were significantly higher than those in control group (P < 0.05). Compared with the control group, Caspase-12 antigen-positive cells increased significantly at 24 and 48 h after hyperoxia. The apoptosis index of P10 and P12 hyperoxia group was higher than that of control group (18.742 ± 2.503 vs 4.587 ± 2.353, 36.184 ± 3.655 vs 5.351 ± 2.678), the difference was statistically significant (P <0.05). Conclusion Hyperoxia exposure can lead to white matter damage of corpus callosum in neonatal mice, which may lead to over apoptosis of corpus callosum white matter cells by increasing Caspase-12 expression, leading to white matter damage of corpus callosum.