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本实验研究慢性缺氧对大鼠延髓呼吸中枢的损伤作用,并探讨其损伤作用是否与氧化应激和细胞凋亡有关。健康雄性SD大鼠,随机分为两组:空气对照组和慢性缺氧组。采用尼氏染色法,观察慢性缺氧对延髓呼吸中枢神经元的损伤;采用生物化学方法,检测延髓丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活力,观察慢性缺氧对延髓氧化应激水平的影响;采用RT-PCR方法,检测延髓Bax mRNA和Bcl-2mRNA的表达,观察慢性缺氧对延髓细胞凋亡水平的影响。结果显示:与空气对照组相比,在慢性缺氧组大鼠延髓,pre-BtC、Amb、NTS、FN、12N等呼吸相关核团尼氏染色光密度值均降低(P<0.05);MDA含量增加(P<0.05),SOD活力无显著变化(P>0.05);Bcl-2mRNA水平降低(P<0.05),Bax mRNA水平无显著差异(P>0.05)。研究表明,慢性缺氧对呼吸中枢有严重损伤,这种损伤可能与其增强氧化应激和促进细胞凋亡等作用有关。
In this study, chronic hypoxia on the respiratory center of the medulla oblongata injury and explore whether its injury is related to oxidative stress and apoptosis. Healthy male SD rats were randomly divided into two groups: air control group and chronic hypoxia group. The Nissl staining was used to observe the damage of central neurons in the medulla oblongata caused by chronic hypoxia. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in the medulla oblongata were measured by biochemical methods. On the level of oxidative stress in the medulla oblongata. The expression of Bax mRNA and Bcl-2 mRNA in the medulla oblongata was detected by RT-PCR, and the effect of chronic hypoxia on the apoptosis of the medulla oblongata was observed. The results showed that compared with the air control group, the Nissl staining optical density of pre-BtC, Amb, NTS, FN, 12N and other respiratory-related nuclei in the chronic hypoxia group were decreased (P <0.05) (P <0.05); the activity of SOD had no significant change (P> 0.05); the level of Bcl-2 mRNA decreased (P <0.05); the level of Bax mRNA had no significant difference (P> 0.05). Studies have shown that chronic hypoxia has severe respiratory center injury, this damage may be related to its role in enhancing oxidative stress and promote apoptosis.