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目的 研究短暂缺氧、血清剥夺复氧复注血清 (再灌流 )后神经细胞顿抑现象及其可能机制。方法 将PC12细胞随机分为正常对照组和缺氧组,每组根据不同的再灌流时间又分为 3个亚组 (缺氧组分别为缺氧 15min再灌流 1h组、3h组、6h组,正常对照组各亚组的时间点与缺氧组相对应)。测定短暂缺氧血清剥夺再灌流后不同时间点的三磷酸腺苷含量、线粒体膜电位和细胞活性。结果 与正常对照组相比,缺氧血清剥夺 15min再灌流 1h后的三磷酸腺苷含量(1. 05±0. 34)、线粒体膜电位(41. 39±1. 242)和细胞活性 (0. 809±0. 087)显著降低 (P<0. 05),且于再灌流 6h后基本恢复至正常水平。结论 短暂缺氧血清剥夺再灌流后,存在低能量状态,且可完全恢复,表明可能存在神经细胞顿抑现象,其原因可能与再灌流后线粒体呼吸链上的琥珀酸脱氢酶等活性下降及线粒体的膜电位变化等有关。
Objective To study the phenomenon of stunned neural cells after transient hypoxia, serum deprived of reoxygenation and reperfusion serum (reperfusion) and its possible mechanism. Methods PC12 cells were randomly divided into normal control group and hypoxia group. Each group was divided into three subgroups according to different reperfusion time: hypoxia group were reperfused for 1 hour, 3 hours, 6 hours, The normal control group of each sub-group of time points and hypoxia group corresponding). The levels of adenosine triphosphate, mitochondrial membrane potential and cell viability at different time points after transient hypoxic serum deprivation and reperfusion were determined. Results Compared with the normal control group, the content of adenosine triphosphate (1. 05 ± 0.34), mitochondrial membrane potential (41.39 ± 1.242) and cell viability (0.809 ± 0. 087) (P <0.05), and returned to normal level 6 h after reperfusion. Conclusions After a brief hypoxia serum deprivation and reperfusion, there is a low energy state and can be completely recovered, indicating that there may be stunned neuronal cells. The reason may be related to the decrease of activity of succinate dehydrogenase on the respiratory chain of mitochondria after reperfusion Mitochondrial membrane potential changes and so on.