摘要
目的:研究MFA对大鼠脑缺血再灌注损伤的作用.方法:用四动脉结扎法造成大鼠急性全脑缺血再灌损伤.MFA在缺血和再灌前5 min分别iv 20 mg kg^(-1).结果:再灌组的脑水份含量显著增高(82.7％±1.1％vs对照组79.7％±0.5％;P<0.01),MFA能抑制这一水肿(80.9％±0.9％,vs再灌组P<0.01).再灌组的CK含量下降明显(4.7±1.4 vs对照组8.4±1.2 U/mg protein,P<0.01),MFA能减少这下降(7.2±1.1 U/mg protein vs再灌组P<0.01).再灌组能引起脂质过氧化物MDA含量的增加(2.3±0.5vs对照组1.5±0.4 nmol/mg protein,P<0.01和SOD的减少(3.1±1.6vs对照组10.5±3.9U/mg protein P<0.01),而MFA则抑制MDA的升高(1.6±0.4 nmol/mg protein vs再灌组P<0.05),同时保护了SOD的活性(7.9±1.6 U/mg protein vs再灌组P<0.01). 结论:MFA能保护急性脑缺血再灌损伤,而此作用可能与保护内源性自由基清除系统、抑制脂质过氧化有关.
To examine the possible beneficial action of methylflavonolamine (MFA) on cerebral ischemia/reperfusion injury. METHODS: Acute cerebral ischemia-reperfusion injury was produced by 4-vessel occlusion and subsequent 1-h release. MFA, 20 mg kg-1, was injected intravenously 5 min before occlusion and again before release. RESULTS: The brain water content in the reperfusion group (Rep) was elevated (82.7 %±1.1% vs control 79.7 %±0. 5 % , P<0. 01) , while MFA alleviated the brain edema (80. 9% ±0. 9 % vs Rep, P<0. 01). The CK level ofbrain tissue in Rep decreased (4.7±1.4 vs control 8.4±1.2 U/mg protein, P<0. 01), but MFA restored it (7.2±1.1U/mg protein vs Rep, P<0. 01). Reperfusion caused the rise of lipid peroxides ( 2.3±0. 5 vs control 1.5±0. 4 nmol/mg protein, P< 0. 01) and weakened the superoxide dismutase (SOD) (3.1±1. 6 vs control 10.5±3. 9 U/mg protein P<0. 01), MFA reduced the rise of lipid peroxides (1.6±0.4 nmol/mg protein vs Rep, P<0. 05) and protected the activity of SOD (7. 9±1.6 U/mg protein vs Rep, P<0. 01) in brain. CONCLUSION: MFA has the protective effects on cerebral ischemia/reperfusion, and these effects are relative to scavenging free radicals and anti-lipid peroxidation.
出处
《中国药理学报》
CSCD
1995年第4期304-307,共4页
Acta Pharmacologica Sinica
关键词
甲基黄酮醇胺
脑缺血
再灌注损伤
自由基
药理
methylflavonolamine
cerebral ischemia
reperfusion injury
brain edema
creatine kinase
free radicals
superoxide dismutase
lipid peroxides
