摘要
用原代培养大鼠皮质神经细胞的方法，观察ｌ丁基苯酞（ｌＮＢＰ）和ｄ丁基苯酞（ｄＮＢＰ）对ＫＣｌ及Ｎ甲基Ｄ门冬氨酸（ＮＭＤＡ）诱导的大鼠皮质神经细胞损伤的保护作用。结果表明：ｌＮＢＰ和ｄＮＢＰ能剂量依赖性地抑制ＮＭＤＡ诱导的大鼠皮质神经细胞内乳酸脱氢酶的释放，降低细胞死亡率，改善受损细胞的形态；此外ｌＮＢＰ和ｄＮＢＰ还能明显减轻ＫＣｌ诱导的神经细胞损伤。提示：ｌＮＢＰ和ｄＮＢＰ对ＫＣｌ及ＮＭＤＡ诱导的大鼠皮质神经细胞损伤有明显保护作用。
The protective effects of l 3 n butylphthalide( l NBP) and d 3 n butylphthalide( d NBP) on KCl(20 mmol·L -1 ) or NMDA( N methyl D aspartate, 30 μmol·L -1 ) induced cytotoxicity in primary cultured rat cortical neurons were studied. Intracellular LDH release, percentage of cell death and cellular morphological changes were used to evaluate the effect of drugs. l NBP(1～100 μmol·L -1 ) and d NBP(1～100 μmol·L -1 ), but not nimodipine (1～100 μmol·L -1 ), were shown to dose dependently inhibit LDH release induced by NMDA (30 μmol·L -1 ) in cultured rat cortical neurons with IC 50 values of 4 89 μmol·L -1 and 13 52 μmol·L -1 , respectively. The percent cell death was reduced with IC 50 values of 44 37 and 49 78 μmol·L -1 , and the cellular morphology improved. The effect seemed to be the same as that of equal concentration of NAME( N G nitro L arginine methyl ester). In addition, l NBP(10 μmol·L -1 ), d NBP(10 μmol·L -1 ) and nimodipine(10 μmol·L -1 ) also produced significant inhibition on intracellular LDH release and decrease in percent cell death induced by KCl(20 mmol·L -1 ) in cultured neurons. The potencies of l NBP and d NBP were similar to that of equal dose of nimodipine. These data suggest that l NBP and d NBP can remarkably protect cultured neurons against the damage induced by KCl and NMDA.
出处
《药学学报》
CAS
CSCD
北大核心
1997年第5期340-346,共7页
Acta Pharmaceutica Sinica
基金
国家科委1035工程重大项目基金
关键词
丁基苯酞
脑缺血
乳酸脱氢酶
尼莫地平
药物疗法
l
3 n Butylphthalide
d
3 n Butylphthalide
LDH
Cortical neuronal culture
Nimodipine
N G nitro L arginine methyl ester
