丹酚酸A对大鼠脑突触体和线粒体氧应激损伤的体外保护作用

利用蔗糖梯度法分离大鼠脑突触体和线粒体，以Fe^2＋-半胱氨酸（Cys）为氧自由基生成系统造成大鼠脑突触体和线粒体氧应激损伤模型. 在体外Fe^2＋-Cys与脑突触体和线粒体共同温孵可使丙二醛(MDA)生成量显著增加，线粒体ATP酶活性下降. 预先加入丹酚酸 A(Sal A)可显著抑制MDA生成，恢复线粒体 ATP酶活性，防止线粒体肿胀和膜流动性的降低. 通过电镜照片可看到Fe^2＋-Cys引起的线粒体和突触体结构病理性改变，预先加入Sal A可减轻Fe^2＋-Cys造成的这一损伤. 此外，Sal A可阻抑H₂O₂引起的脑突触体GSH含量的降低. 由此可见，Sal A体外对氧应激引起的大鼠脑突触体和线粒体脂质过氧化损伤有明显的保护作用.

The in vitro protective effect of salvainolic acid A on oxidative stress induced injury of rat cerebral mitochondria and synaptosomes

The aging brain undergoes a process of enhanced oxidative stress injury. The aim of this work was to investigate the effects of salvianolic acid A (Sal A) on oxidative stress induced injury of rat cerebral mitochondria and synaptosomes in vitro. Incubation of cerebral mitochondria and synaptosomes with Fe^2＋-cysteine(Cys) at 37℃ resulted in an increase in malondialdehyde (MDA) formation and a decrease in ATPase activity. Sal A (100 μmol·L^-1) completely inhibited the peroxidative stress induced increase in MDA formation of mitochondria and synaptosomes, at the same time the ATPase activity of mitochondria increased. The swelling of mitochondria as well as reduction of membrane fluidity of mitochondria and synaptosomes induced by Fe^2＋-Cys were also prevented by Sal A. Sal A(10 μmol·L^-1) significantly inhibited decrease in synaptosome glutathion (GSH) content induced by H₂O₂. The electron micrographs also showed that Sal A could reduce the pathological damage of mitochondria and synaptosomes induced by Fe^2＋-Cys. The results suggest that Sal A have protective action against oxidative stress induced injury of rat cerebral mitochondria and synaptosomes in vitro.