论文部分内容阅读
目的探讨早期常压高氧治疗对大鼠颅脑损伤后线粒体功能及细胞凋亡的保护作用及其机制。方法将成年健康雄性大鼠分为假手术组、模型组、高压氧组及常压氧组,每组28只。于伤后1周行神经功能缺损评分,并检测线粒体膜电位(MMP)、丙二醛(MDA)和超氧化物歧化酶(SOD)的变化。观察各组电镜下线粒体形态,并采用原位缺口末端标记(TUNEL)法检测神经细胞凋亡情况。结果四组间神经功能缺损评分比较差异有统计学意义(F=3.682,P=0.039),且常压氧组与高压氧组较模型均明显改善(P均<0.05)。四组间MMP、MDA、SOD及阳性细胞计数比较,差异均有统计学意义(F=8.571、12.4、6.604、9.425,P均<0.05),与模型组比较,常压氧组及高压氧组的MMP均明显升高,MDA、SOD及阳性细胞计数均明显下降(P均<0.05),而高压氧组与常压氧组的MMP、MDA、SOD及阳性细胞计数比较,差异均无统计学意义(P均>0.05)。电镜下,模型组线粒体膜出现断裂、形态较大、肿胀明显,线粒体内出现空泡化,线粒体嵴消失;而常压氧及高压氧组线粒体膜基本完整,肿胀程度较模型组轻微,线粒体嵴尚存在,未见明显空泡化现象,且后两者线粒体形态差异不明显。结论早期常压氧治疗通过保护线粒体结构和功能从而抑制缺血半影区的细胞凋亡,以促进大鼠脑外伤后的神经功能的恢复。
Objective To investigate the protective effect of early atmospheric hyperoxia treatment on mitochondrial function and apoptosis after traumatic brain injury in rats and its mechanism. Methods Male adult rats were divided into sham operation group, model group, hyperbaric oxygen group and normobaric oxygen group, 28 in each group. Neurological deficit scores were performed 1 week after injury and the changes of mitochondrial membrane potential (MMP), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected. The morphology of mitochondria in each group was observed under electron microscope. The apoptosis of nerve cells was detected by TUNEL method. Results There was significant difference in the score of neurological deficit between the four groups (F = 3.682, P = 0.039), and the levels of normobaric oxygen and hyperbaric oxygen were significantly improved (all P <0.05). There were significant differences in MMP, MDA, SOD and positive cell counts between the four groups (F = 8.571,12.4,6.604,9.425, P <0.05). Compared with the model group, the normobaric oxygen group and hyperbaric oxygen group (P <0.05). However, there was no significant difference in MMP, MDA, SOD and positive cell counts between hyperbaric oxygen group and normobaric oxygen group Significance (P> 0.05). Under the electron microscope, the mitochondrial membrane in the model group was broken, its shape was bigger and the swelling was obvious. The mitochondria vacuoles and the mitochondrial cristae disappeared. The mitochondrial membrane in the normobaric oxygen and hyperbaric oxygen groups were basically intact, Still exists, no obvious vacuoles, and the latter two mitochondrial morphology is not obvious. Conclusions Early treatment with normobaric oxygen can inhibit the apoptosis in the penumbra of the ischemic area by protecting the structure and function of mitochondria, so as to promote the recovery of neurological function after traumatic brain injury in rats.