（E）-3-（4-（2-（二甲氨基）乙氧基）-3-甲氧苯基）丙烯酸对大鼠局灶性脑缺血的保护作用及机制

目的：研究（E）-3-（4-（2-（二甲氨基）乙氧基）-3-甲氧苯基）丙烯酸（DEAAA）对大鼠局灶性脑缺血的保护作用及作用机制。方法：建立大鼠大脑中动脉阻塞模型（MCAO）,以奥扎格雷为阳性对照组,观察DEAAA各剂量组（30、18、10.8mg/kg）对脑缺血大鼠神经行为、脑含水量、脑梗死面积、脑组织生化指标和脑组织病理变化的影响。结果：DEAAA（30、18mg/kg）可显著降低脑水肿程度,减少脑梗死面积（P〈0.05和P〈0.01vs缺血模型组）,并增加MCAO大鼠脑组织超氧化物歧化酶含量、升高乳酸脱氢酶活力并且降低丙二醛水平（P〈0.05和P〈0.01vs缺血模型组）,明显改善大鼠神经行为（P〈0.05和P〈0.01vs缺血模型组）,改善脑组织神经细胞缺血后的病理改变。结论：DEAAA对脑缺血大鼠有保护作用,其机制可能与抗氧化、提高自由基清除能力、增强脑组织抵抗缺氧能力有关。

Protective effects and the mechanisms of DEAAA on focal cerebral ischemia in rats

AIM：To study the protective effects of （E）-3-（4-（2-（dimethylamino） ethoxyl）-3-anisyl） acrylic acid（DEAAA） on focal cerebral ischemia of rats. METHODS：Middle cerebral artery occlusion（MCAO） model was used to evaluate the drug＇s effects. With Ozagrel as a positive control drug,after cerebral ischemia,the effect of different doses of DEAAA on the neurological behaviors,the cerebral water volumes,the cerebral infarction areas,the cerebral biochemistry and the pathologic change of brains were evaluated. RESULTS：DEAAA （30,18 mg/kg） decreased the cerebral water volumes and the cerebral infarction areas（P〈0.05,P〈0.01）,increased the levels of SOD and LDH,decreased the content of MDA in brain（P〈0.05,P〈0.01）,improved neurological behaviors of the MCAO rats（P〈0.05,P〈0.01） and improved the pathologic change of brain after cerebral ischemia. CONCLUSION：DEAAA has the protective effects on cerebral ischemia in rats,the mechanisms of DEAAA involved in anti-oxidation,improving energy metabolism and increasing the ability of getting rid of free radicals.