淫羊藿苷对氧自由基所致大鼠脑线粒体损伤的保护作用

Protective effect of icariin against mitochondrial damage induced by oxygen free radical in rat cerebral cells

目的设想神经元缺氧损伤与自由基损伤线粒体有关,由此探讨淫羊藿苷的保护作用机制。方法采用Fe2+/维生素C(VitC)为氧自由基生成系统建立氧自由基损伤线粒体的体外模型。观察淫羊藿苷对线粒体肿胀度、呼吸链复合体酶Ⅰ～Ⅳ活性、丙二醛(MDA)含量的影响。结果Fe2+/VitC(1mmol·L-1/1mmol·L-1,10mmol·L-1/10mmol·L-1)可使线粒体的肿胀度和MDA含量显著增加,呼吸链复合体酶Ⅱ～Ⅳ活性不同程度下降。预先加入淫羊藿苷(0.03和0.1mg·L-1)能显著抑制线粒体肿胀,减少MDA含量,提高呼吸链复合体酶Ⅱ～Ⅳ的活性。结论淫羊藿苷对氧自由基损伤的大鼠脑线粒体呼吸链具有保护作用。

AIM To investigate the mechanism of protective effects of icariin with the hypothesis that hypoxia-induced neuron injury is related to oxygen free radical-induced mitochondrial damage. METHODS The mitoehondria were damaged by oxygen free radical derived from ferrous sulfate/vitamin C （Fe^2＋/VitC） in vitro. The mitochondrial swelling, activitv of complex Ⅰ-complex Ⅳ and the content of malondialdehvde （MDA） were measured. RESULTS The swelling and content of MDA of mitochondria were significantly increased, and activities of complex Ⅱ-complex Ⅳ, of mitochondria were decreased in model group induced by 1 mmol·L^-1 Fe^2＋/1 mmol·L^-1 VitC or 10 mmol·L^-1 Fe^2＋/10 mmol·L^-1 VitC. Pretreating mitochondria with icariin （0.03 and 0.1 mg·L^-1） obviously decreased swelling and content of MDA. and significantly increased activities of complex Ⅱ-complex Ⅳ. CONCLUSION Icariin has protective effect on rat cerebral mitochondria injury induced by oxygen free radical.