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目的观察大鼠脑出血后神经细胞线粒体DNA(mtDNA)缺失突变与氧化应激水平的相关性。方法 SD大鼠110只,随机分为正常组10只,脑出血组和假手术组各50只,Rosenherg法建立大鼠脑出血模型,后2组术后12h、1、2、4和7 d时观察,每个时间点10只,巢氏PCR技术检测大鼠神经细胞mtDNA缺失突变率,荧光实时定量PCR技术定量分析mtDN~(4834 bp)缺失含量,硫代巴比妥酸比色法和黄嘌呤氧化法检测脑组织丙二醛含量、超氧化物歧化酶(SOD)活性。结果脑出血组大鼠神经细胞mtDNA~(4834 bp)片断缺失总发生率54%,明显高于假手术组(P<0.0)5);与假手术组相应时间点比较,脑出血组神经细胞mtDNA~(4834 bp)平均缺失率明显升高(P<0.05);与假手术组和正常组比较,脑出血组SOD活性明显降低,丙二醛含量明显升高(P<0.05)。结论大鼠脑出血后,mtDNA~(4834 bp)缺失与氧化应激水平相关,mtDNA~(4834 bp)缺失突变可能是脑出血后迟发性神经细胞损伤机制之一。
Objective To observe the correlation between mitochondrial DNA (mtDNA) deletion mutation and oxidative stress in rat brain after intracerebral hemorrhage. Methods 110 SD rats were randomly divided into normal group (n = 10), cerebral hemorrhage group (n = 50) and sham operation group (n = 50). Rosenherg method was used to establish intracerebral hemorrhage model in rats. 10 rabbits were observed at each time point. The mutation rate of mtDNA in rat neurons was detected by nested PCR. Quantitative analysis of mtDN ~ (4834 bp) deletion, thiobarbituric acid colorimetry and The contents of malondialdehyde and the activity of superoxide dismutase (SOD) in brain tissue were detected by xanthine oxidation method. Results The total deletion rate of mtDNA ~ (4834 bp) was 54% in cerebral hemorrhage group, which was significantly higher than that in sham operation group (P <0.05). Compared with the sham operation group, the number of neuronal cells The mean deletion rate of mtDNA ~ (4834 bp) was significantly increased (P <0.05). Compared with sham operation group and normal control group, SOD activity was significantly decreased and MDA content was significantly increased in cerebral hemorrhage group (P <0.05). Conclusion The loss of mtDNA ~ (4834 bp) is related to oxidative stress after intracerebral hemorrhage in rats. The deletion of mtDNA ~ (4834 bp) may be one of the mechanisms of delayed neuronal injury after intracerebral hemorrhage.