Shen J, Wang J, Zhao B, Hou J, Gao T, Xin W
Institute of Biophysics Academia Sinica, Beijing 100101, China.
Biochim Biophys Acta. 1998 Apr 28;1406(3):228-36. doi: 10.1016/s0925-4439(98)00007-6.
The cardioprotective effects of EGb 761 on the release of nitric oxide (NO), the concentration of serum thiobarbituric acid reaction substance (TBARS), the activity of creatine kinase (CK) and the incidence of ventricular arrhythmias were investigated in myocardial ischemia-reperfusion injury in vivo. Using sodium nitrite (NaNO2) as standard source of nitric oxide (NO), we compared the correlation coefficients of the three measuring methods used currently in the determination of NOFe2+(DETC)2 complex with that of the measuring method suggested in this study. The result showed that measuring the whole height of three splitting signals is the best linear correlation to the concentration of NO comparing with other methods in this system. Using this method, we observed the effects of EGb 761 on NOFe2+(DETC)2 complex in myocardial ischemia-reperfusion injury in vivo. The hearts of the Wistar rats were subjected to 30 min of ischemia and 10 min of reperfusion in vivo. Different doses of EGb 761 (25, 50, 100, 200 mg/kg i.p.), superoxide dismutase (SOD, 10(4) U/kg), l-arginine (50 mg/kg i.p.) and nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine (NNA, 50 mg/kg i.p.) were administered to the ischemia-reperfusion rats. EGb 761 under the dose of 100 mg/kg increased the signal intensity of NOFe2+(DETC)2 complex, while EGb 761 at 200 mg/kg showed an effect of decreasing the signal intensity of NOFe2+(DETC)2 complex. EGb 761 inhibited the formation of TBARS, the release of CK, and mitigated the incidence of ventricular arrhythmias in a dose dependent way. Both l-arginine and SOD increased the signal intensity of NOFe2+(DETC)2 complex and inhibited the formation of TBARS, the leakage of CK and the incidence of ventricular arrhythmia. NNA not only had no protective effects on myocardial injury, but also increased the incidence of reperfusion-induced arrhythmia. In conclusion, EGb 761 has cardiovascular protective effects by means of adjusting the level of NO and inhibiting oxygen free radicals induced lipid peroxidation in myocardial ischemia-reperfusion injury in vivo.
在体内心肌缺血再灌注损伤模型中，研究了银杏叶提取物761（EGb 761）对一氧化氮（NO）释放、血清硫代巴比妥酸反应物质（TBARS）浓度、肌酸激酶（CK）活性及室性心律失常发生率的心脏保护作用。以亚硝酸钠（NaNO2）作为一氧化氮（NO）的标准来源，比较了目前测定NOFe2+(DETC)2复合物的三种测量方法与本研究建议的测量方法的相关系数。结果表明，在该系统中，与其他方法相比，测量三个分裂信号的总高度与NO浓度具有最佳线性相关性。采用该方法，观察了EGb 761对体内心肌缺血再灌注损伤中NOFe2+(DETC)2复合物的影响。对Wistar大鼠心脏进行30分钟缺血和10分钟再灌注处理。向缺血再灌注大鼠腹腔注射不同剂量的EGb 761（25、50、100、200mg/kg）、超氧化物歧化酶（SOD，10(4)U/kg）、L-精氨酸（50mg/kg腹腔注射）和一氧化氮合酶（NOS）抑制剂NG-硝基-L-精氨酸（NNA，50mg/kg腹腔注射）。100mg/kg剂量的EGb 761增加了NOFe2+(DETC)2复合物的信号强度，而200mg/kg的EGb 761则显示出降低NOFe2+(DETC)2复合物信号强度的作用。EGb 761以剂量依赖性方式抑制TBARS的形成、CK的释放，并减轻室性心律失常的发生率。L-精氨酸和SOD均增加了NOFe2+(DETC)2复合物的信号强度，并抑制了TBARS的形成、CK的泄漏和室性心律失常发生率。NNA不仅对心肌损伤无保护作用，反而增加了再灌注诱导的心律失常发生率。总之，EGb 761通过调节NO水平和抑制体内心肌缺血再灌注损伤中氧自由基诱导的脂质过氧化发挥心血管保护作用。
