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目的:观察银杏叶提取物EGb761对外源性自由基所致离体心脏损伤的保护作用及其机制。方法:离体大鼠心脏采用Langengoff灌流法,记录心率(HR)、冠脉流量(CF)、左室内压(LVP)和左室内压变化最大速率+dp/dtmax,测定肌酸激酶(CK)释放量和心肌组织丙二醛(MDA)和一氧化氮(NO)含量。结果:以含0.25 mol.L-11.1-二苯基-三硝基苯肼(DPPH)的K-H液灌流心脏10 min可显著损伤心功能,表现LVP和+dp/dtmax降低,增加心肌组织CK释放和MDA含量以及NO水平的降低;实验前24 h单次灌胃给予EGb761(100 mg.kg-1)可显著改善DPPH所致的心功能(LVP和+dp/dtmax)损伤,抑制心肌组织CK释放和MDA含量的增加以及NO水平的降低。预先给予NO合酶抑制剂L-NAMA(5 mg.kg-1)、蛋白激酶C(PKC)抑制剂Calphostin C或心肌细胞膜ATP敏感钾通道(sarcKATP)阻断药HMR1883(3 mg.kg-1),均可明显抑制EGb761对DPPH所致心功能损伤的保护作用。结论:EGb761对DPPH所致大鼠心肌损伤具有保护作用,这一保护作用可能与增加NO合成、激活PKC从而引起sarcKATP通道开放有关。
Objective: To observe the protective effect of Ginkgo biloba extract EGb761 on exogenous free radical-induced heart damage and its mechanism. METHODS: Langendorff perfusion method was used on isolated rat heart to record heart rate (HR), coronary flow (CF), left ventricular pressure (LVP) and maximum rate of left ventricular pressure change + dp/dtmax. Creatine kinase (CK) was measured. The amount of release and myocardial tissue malondialdehyde (MDA) and nitric oxide (NO) content. RESULTS: Perfusion of the heart with KH solution containing 0.25 mol.L-11.1-diphenyl-trinitrophenylhydrazine (DPPH) for 10 min significantly impaired cardiac function, demonstrated decreased LVP and +dp/dtmax, and increased myocardial CK release. The decrease of MDA content and NO level; single administration of EGb761 (100 mg.kg-1) 24 h before the experiment significantly improved DPPH-induced heart function (LVP and +dp/dtmax) damage and inhibited myocardial tissue CK Release and increase in MDA content and reduction in NO levels. Pre-administered NO synthase inhibitor L-NAMA (5 mg.kg-1), protein kinase C (PKC) inhibitor Calphostin C, or cardiac membrane ATP-sensitive potassium channel (sarcKATP) blocker HMR1883 (3 mg.kg-1 ), can significantly inhibit the EGb761 on DPPH-induced heart damage protection. CONCLUSION: EGb761 has a protective effect on DPPH-induced myocardial injury in rats. This protective effect may be related to increased NO synthesis, activation of PKC and thus the opening of sarcKATP channels.