中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2010年
9期
905-908
,共4页
异丙酚%线粒体%脑缺血再灌注
異丙酚%線粒體%腦缺血再灌註
이병분%선립체%뇌결혈재관주
Propofol%Mitochondria%Cerebral ischemia and reperfusion
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.
目的 探討靜脈痳醉藥異丙酚對腦缺血再灌註損傷模型大鼠的神經保護作用.方法 SD大鼠48隻按隨機數字錶法分為假手術組、模型組、50 mg/kg異丙酚和100 mg/kg異丙酚組,每組12隻.後3組大鼠均製備腦缺血(2 h)再灌註(24 h)模型,恢複灌註後分彆經腹腔內註射等體積生理鹽水和50、100 mg/kg異丙酚.再灌註24 h後對大鼠進行神經功能缺損評分,應用TTC染色觀察腦梗死的範圍,化學比色法檢測腦組織線粒體琥珀痠脫氫酶(SDH)、Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶活性的改變.結果 與模型組比較,50、100mg/kg異丙酚組大鼠神經功能缺損評分較低,腦組織線粒體SDH、Na+-K+-ATP酶、Ca2+Mg2+-ATP酶活性增高,差異有統計學意義(P＜0.05);與50mg/kg異丙酚組[(45.9±25.1)U/mg pro,(5.24±0.85)分]比較,100mg/kg異丙酚組SDH活性[(96.1±20.8)U/mgpro]較高,神經功能缺損評分(4.40±0.79)較低,差異有統計學意義(P＜0.05).結論異丙酚對腦缺血再灌註損傷大鼠具有神經保護作用,促進線粒體SDH、Na+-K+-ATP酶、Ca2+Mg2+-ATP酶活性的恢複、保護線粒體功能是其機製之一.
목적 탐토정맥마취약이병분대뇌결혈재관주손상모형대서적신경보호작용.방법 SD대서48지안수궤수자표법분위가수술조、모형조、50 mg/kg이병분화100 mg/kg이병분조,매조12지.후3조대서균제비뇌결혈(2 h)재관주(24 h)모형,회복관주후분별경복강내주사등체적생리염수화50、100 mg/kg이병분.재관주24 h후대대서진행신경공능결손평분,응용TTC염색관찰뇌경사적범위,화학비색법검측뇌조직선립체호박산탈경매(SDH)、Na+-K+-ATP매、Ca2+-Mg2+-ATP매활성적개변.결과 여모형조비교,50、100mg/kg이병분조대서신경공능결손평분교저,뇌조직선립체SDH、Na+-K+-ATP매、Ca2+Mg2+-ATP매활성증고,차이유통계학의의(P＜0.05);여50mg/kg이병분조[(45.9±25.1)U/mg pro,(5.24±0.85)분]비교,100mg/kg이병분조SDH활성[(96.1±20.8)U/mgpro]교고,신경공능결손평분(4.40±0.79)교저,차이유통계학의의(P＜0.05).결론이병분대뇌결혈재관주손상대서구유신경보호작용,촉진선립체SDH、Na+-K+-ATP매、Ca2+Mg2+-ATP매활성적회복、보호선립체공능시기궤제지일.
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.
