CAJ | 학술논문

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。
목적：탐토조기상압고양치료대대서로뇌손상후선립체공능급세포조망적보호작용급기궤제。방법장성년건강웅성대서분위가수술조、모형조、고압양조급상압양조，매조28지。우상후1주행신경공능결손평분，병검측선립체막전위（MMP）、병이철（MDA）화초양화물기화매（SOD）적변화。관찰각조전경하선립체형태，병채용원위결구말단표기（TUNEL）법검측신경세포조망정황。결과사조간신경공능결손평분비교차이유통계학의의（F＝3.682，P＝0.039），차상압양조여고압양조교모형균명현개선（P균<0.05）。사조간MMP、MDA、SOD급양성세포계수비교，차이균유통계학의의（F＝8.571、12.4、6.604、9.425，P균<0.05），여모형조비교，상압양조급고압양조적MMP균명현승고，MDA、SOD급양성세포계수균명현하강（P균<0.05），이고압양조여상압양조적MMP、MDA、SOD급양성세포계수비교，차이균무통계학의의（P균>0.05）。전경하，모형조선립체막출현단렬、형태교대、종창명현，선립체내출현공포화，선립체척소실；이상압양급고압양조선립체막기본완정，종창정도교모형조경미，선립체척상존재，미견명현공포화현상，차후량자선립체형태차이불명현。결론조기상압양치료통과보호선립체결구화공능종이억제결혈반영구적세포조망，이촉진대서뇌외상후적신경공능적회복。
Objective To investigate the protective effect and its mechanism of early normobaric hyperoxia therapy on mitochondrial function and apoptosis after craniocerebral trauma in rats. Methods Adult male SD rats were randomly divided into the sham operation group, model group, normobaric hyperoxia group and hyperbaric oxygen group, 28 rats in each group. The neurological severity score, mitochondrial membrane potential (MMP), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected, and the mitochondrial morphology was observed by electron microscopy in ischemic penumbra seven days after injury. The TdT-mediated dUTP nick end labeling (TUNEL) was used to test the neural cell apoptosis. Results There were significant differences of the neurological severity score among the four groups (F=3.682, P=0.039), and the scores in the normobaric hyperoxia and hyperbaric oxygen groups were better than that in the model group (all P<0.05). The levels of MMP, MDA and SOD and TUNEL positive cells were significantly different among the four groups (F = 8.571, 12.400, 6.604, 9.425; all P<0.05). In the normobaric hyperoxia and hyperbaric oxygen groups, the levels of MMP were lower, the levels of MDA and SOD and TUNEL positive cells were higher than those in the model group (all P<0.05). However, the levels of MMP, MDA and SOD and TUNEL positive cells had no statistical significance between the normobaric hyperoxia and hyperbaric oxygen groups (all P > 0.05). In the mitochondrial morphology, mitochondrial membrane were ruptured, larger, swelling, cavitation occurred, and mitochondrial cristae disappeared in the model group. In the normobaric hyperoxia and hyperbaric oxygen groups, mitochondrial membrane were complete and mild swelling, the mitochondrial crest still existed and no obvious cavitation. Conclusion Early normobaric hyperoxia therapy can promote the recovery of neurological function after craniocerebral trauma in rats, and its possible mechanism is to inhibit apoptosis in ischemic penumbra by improving mitochondrial function.