异丙酚对大鼠脑缺血再灌注损伤线粒体能量代谢的影响

Effects of propofol on mitochondrial energy metabolism of rats with cerebral ischemiareperfusion injury

目的 探讨静脉麻醉药异丙酚对脑缺血再灌注损伤模型大鼠的神经保护作用.方法 SD大鼠48只按随机数字表法分为假手术组、模型组、50 mg/kg异丙酚和100 mg/kg异丙酚组,每组12只.后3组大鼠均制备脑缺血（2 h）再灌注（24 h）模型,恢复灌注后分别经腹腔内注射等体积生理盐水和50、100 mg/kg异丙酚.再灌注24 h后对大鼠进行神经功能缺损评分,应用TTC染色观察脑梗死的范围,化学比色法检测脑组织线粒体琥珀酸脱氢酶（SDH）、Na＋-K＋-ATP酶、Ca2＋-Mg2＋-ATP酶活性的改变.结果 与模型组比较,50、100mg/kg异丙酚组大鼠神经功能缺损评分较低,脑组织线粒体SDH、Na＋-K＋-ATP酶、Ca2＋Mg2＋-ATP酶活性增高,差异有统计学意义（P＜0.05）;与50mg/kg异丙酚组[（45.9±25.1）U/mg pro,（5.24±0.85）分]比较,100mg/kg异丙酚组SDH活性[（96.1±20.8）U/mgpro]较高,神经功能缺损评分（4.40±0.79）较低,差异有统计学意义（P＜0.05）.结论异丙酚对脑缺血再灌注损伤大鼠具有神经保护作用,促进线粒体SDH、Na＋-K＋-ATP酶、Ca2＋Mg2＋-ATP酶活性的恢复、保护线粒体功能是其机制之一.

Objective To investigate the neuroprotective effect of intravenous anesthetic drug propofol on rats with cerebral ischemia-reperfusion injury. Methods Forty-eight SD rats were equally randomized into sham-operated group, model group, 50 and 100 mg/kg propofol treatment groups （n=12）.Models were induced in the latter 3 groups by performing cerebral ischemia （2 h） and then reperfusion （24 h）; subsequently, they were treated with intraperitoneal injection of saline, 50 and 100 mg/kg propofol, respectively, after the restoration of perfusion. Neurological deficit scale was performed on these rats; application scope of TTC staining of the cerebral infarction was observed; brain chemical colorimetric assay was employed to detect the activity changes of mitochondrial succinate dehydrogenase （SDH）, Na＋-K＋-ATP enzyme and Ca2＋-Mg2＋-ATP enzyme. Results Compared with those in the model group, the scores of neurological deficit scale in the 50 and 100 mg/kg propofol treatment groups were obviously lower, and the activity of brain tissue mitochondrial SDH, Na＋-K＋-ATP enzyme, Ca2＋-Mg2＋-ATP enzyme in the 50 and 100 mg/kg propofol treatment groups was significantly increased （P〈0.05）.Compared with those in the 50 mg/kg propofol treatment group （[45.9±25.1]U/mg pro, [5.24±0.85]）, the SDH activity （[96.1±20.8] U/mg pro） was obviously higher and the scores of neurological deficit scale （4.40±0.79） were significantly lower in the 100 mg/kg propofol treatment group （P〈0.05）. Conclusion Propofol has a protective effect on rats with cerebral ischemia-reperfusion injury by promoting the recovery of activity of mitochondrial SDH, Na＋-K＋-ATP enzyme, Ca2＋-Mg2＋-ATP enzyme to protect the mitochondrial function.