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目的 观察总丹酚酸(total salvianolic acids,Sal)对小鼠脑缺氧的保护作用.方法 利用小鼠断头及亚硝酸钠造成急性脑缺氧模型,观察Sal的抗脑缺氧作用,并以连二亚硫酸钠造成培养神经细胞缺氧损伤模型,初步探讨Sal的作用机制.结果Sal 10,20mg·kg~(-1)iv能明显延长小鼠断头张口喘气时间及亚硝酸钠致缺氧小鼠的生存时间,并显著降低急性脑缺氧小鼠脑组织的丙二醛(MDA)含量.Sal1~10μg·L~(-1)能剂量依赖地降低神经细胞缺氧性损伤时的细胞死亡率,减少乳酸脱氢酶(LDH)的释放,并能明显减少MDA的生成.结论Sal能明显对抗小鼠急性脑缺氧,其机理可能与其减少脂质过氧化物生成有关.
Objective To observe the protective effects of total salvianolic acids (Sal) on cerebral anoxia in mice.Methods Acute cerebral hypoxia model was induced by decapitation and sodium nitrite in mice, The hypoxia injury model of cultured neurons was induced by sodium dithionite and the mechanism of action of Sal was preliminarily discussed.Results Sal 10,20 mg · kg -1 iv could prolong the gasping time of mice with decapitation and the hypoxia induced by sodium nitrite (Superscript +) and decrease the MDA content in the brain of mice with acute cerebral hypoperfusion.Almost 10 ~ 10μg · L -1 of Sal could decrease the cell number of neurons hypoxic injury Reduce the release of lactate dehydrogenase (LDH), and significantly reduce the generation of MDA.Conclusion Sal can obviously antagonize the acute cerebral hypoxia in mice and its mechanism may be related to the reduction of lipid peroxidation.