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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.
Objective: To investigate the effect of MFA on cerebral ischemia-reperfusion injury in rats.Methods: Acute cerebral ischemia-reperfusion injury was induced by four-artery ligation in rats.MFA was given iv 20 mg kg ~ (-1) .Results: The brain water content in reperfusion group was significantly higher (82.7% ± 1.1% vs 79.7% ± 0.5% in control group; P <0.01), and MFA could inhibit this edema (80.9% ± 0.9% (P <0.01, P <0.01 vs control), MFA decreased (7.2 ± 1.1 U / mg, P <0.01) (P <0.01) and the decrease of SOD (P <0.01) in reperfusion group (2.3 ± 0.5 vs control group, 1.5 ± 0.4 nmol / mg protein, vs control group 10.5 ± 3.9U / mg protein P <0.01), while MFA inhibited the increase of MDA (1.6 ± 0.4 nmol / mg protein vs reperfusion group, P <0.05) U / mg protein vs reperfusion group, P <0.01) .Conclusion: MFA can protect against acute cerebral ischemia-reperfusion injury, and this effect may be related to the protection of endogenous free radical scavenging system and inhibition of lipid peroxidation.