Dong Gao-xiang, Feng Yi-Pu
Department of Pharmacology, Institute of Materia Medica, CAMS, PUMC, Beijing 100050, China.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2002 Feb;24(1):93-7.
The aim of the present study was designed to explore the effect of (+/-) -3-n-butylphthalide (NBP) on ATPase, anti-oxidant enzymes activities and lipid peroxidation of mitochondria and cerebral cortex in rats subjected to 24 hours of reperfusion following 2 hours of cerebral ischemia (tMCAO).
Activities of SOD (Superoxide Dismutase), GSH-Px (glutathione Peroxidase,) and CAT (Catalase), and MDA level of mitochondria or cortex were measured by using biochemical methods in tMCAO rats.
(1) The activities of mitochondrial Na+K(+)-ATPase, Ca(2+)-ATPase and Mg2+ ATPase were found to decrease significantly in the vehicle group (ischemia + saline). Pre-treatment with NBP (5, 10, 20 mg/kg, i.p.) 10 min before tMCAO markedly enhanced the activities of Na+K(+)-ATPase and Ca(2+)-ATPase, compared with vehicle group. (2) The activities of SOD and mitochondrial GSH-Px were decreased and MDA level increased in vehicle groups as compared with that in sham group (non-ischemia + saline). NBP (20 mg/kg, i.p.) significantly enhanced total mitochondrial SOD activity, and also enhanced cerebral cortex total SOD activity (in 5, 10, 20 mg/kg groups). However, it had no obvious effect on CuZn-SOD activity. NBP (20 mg/kg i.p.) markedly increased mitochondrial (but not in cerebral cortex) GSH-Px activity; NBP 10, 20 mg/kg markedly decreased mitochondrial MDA level compared with that in vehicle group (P < 0.05). (3) The action of raceme NBP on the increase of the activities of ATPase and antioxidative enzymes seemed to be beneficial than that of (-) -NBP or (+) NBP.
The results suggest that NBP improves energy pump and subsides oxidative injury which may contribute to its anti-neuronal apoptotic effect.
本研究旨在探讨（±）-3-正丁基苯酞（NBP）对大脑中动脉闭塞（tMCAO）2小时后再灌注24小时大鼠线粒体及大脑皮质中ATP酶、抗氧化酶活性和脂质过氧化的影响。
采用生化方法检测tMCAO大鼠线粒体或皮质中SOD（超氧化物歧化酶）、GSH-Px（谷胱甘肽过氧化物酶）、CAT（过氧化氢酶）的活性以及MDA水平。
（1）在溶剂组（缺血+生理盐水）中，线粒体Na+K(+)-ATP酶、Ca(2+)-ATP酶和Mg2+ATP酶的活性显著降低。在tMCAO前10分钟腹腔注射NBP（5、10、20mg/kg）预处理，与溶剂组相比，Na+K(+)-ATP酶和Ca(2+)-ATP酶的活性显著增强。（2）与假手术组（非缺血+生理盐水）相比，溶剂组中SOD和线粒体GSH-Px的活性降低，MDA水平升高。NBP（20mg/kg，腹腔注射）显著增强了线粒体总SOD活性，同时也增强了大脑皮质总SOD活性（5、10、20mg/kg组）。然而，它对CuZn-SOD活性没有明显影响。NBP（20mg/kg，腹腔注射）显著增加了线粒体（而非大脑皮质）GSH-Px活性；与溶剂组相比，NBP 10、20mg/kg显著降低了线粒体MDA水平（P<0.05）。（3）消旋NBP对ATP酶和抗氧化酶活性增加的作用似乎比（-）-NBP或（+）-NBP更有益。
结果表明，NBP可改善能量泵功能并减轻氧化损伤，这可能有助于其抗神经元凋亡作用。
