羟基红花黄色素A对缺血损伤脑组织蛋白质硝基化修饰的影响  

Effect of hydroxysafflor yellow A on protein nitrative modification in brain ischemic injury

作　　者：赵瑞杰[1,2] 孙莉[3] 刘星苗[1] 梁浩[1] 程焱[1] 

机构地区：[1]天津医科大学总医院天津市神经病学研究所,300052 [2]河北省邢台市人民医院神经内二科 [3]天津医科大学总医院天津市神经病学研究所科,300052

出　　处：《中华老年心脑血管病杂志》2013年第2期188-192,共5页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：国家自然科学基金(81070968)

摘　　要：目的研究羟基红花黄色素A(HSYA)对缺血损伤脑组织蛋白质硝基化修饰的影响。方法模拟体内蛋白质硝基化的2条主要途径,体外以BSA为底物,分为对照组及低、中、高干预组(以HSYA 0.01、0.1和1mmol/L干预),Western blot法检测HSYA对BSA硝基化水平的影响。另选SD大鼠45只,随机分为假手术组、模型组和治疗组(HSYA 10mg/kg),每组15只。后2组大鼠制作大脑中动脉闭塞再灌注模型,采用Western blot法、免疫组织化学法观察脑组织蛋白质硝基化水平及HSYA对硝基化修饰的影响;TTC染色观察脑梗死体积的改变。结果与对照组比较,低、中、高干预组蛋白质硝基化水平呈剂量依赖性地降低,以高干预组的抑制作用最明显,差异有统计学意义(P<0.05)。假手术组脑组织中3-硝基酪氨酸仅有少量表达,与假手术组比较,模型组表达明显增加,而治疗组表达较模型组显著下降,差异有统计学意义(P<0.05)。治疗组脑梗死体积较模型组减少48.86%(P<0.01)。结论 HSYA对缺血损伤脑组织蛋白质硝基化具有抑制作用,这可能是其脑缺血再灌注损伤保护作用的分子机制之一。Objective To study the effect of hydroxysafflor yellow A（HSYA） on protein nitrative modification in brain ischemic injury. Methods Two major in vivo protein tyrosine nitration path- ways of HSYA were simulated with bovine serum albumin（BSA） as a substrate. SD rats were di- vided into sham-operation group （control group）, model group, low dose HSYA group, medium dose HSYA group and high dose HSYA group. Effect of HSYA on BSA nitration was detected by Western blot. A rat middle cerebral artery occlusion/reperfusion model was established. Protein nitration in brain tissue and effect of HSYA on nitration modification were detected by Western blot with immunohistochemical staining. Cerebral infarction size was measured with TTC stai ning. Results The protein nitration level was significantly lower in low,medium and high dose HSYA groups,especially in high dose HSYA group than in control group（P〈0.05）, which de creased in a dose-dependent manner. The expression level of 3-nitrotyrosine was very low in con- trol group,significantly higher in model group and significantly lower in HSYA treatment group （P〈0.05）. The cerebral infarction size was smaller in HSYA treatment group（which decreased to 48.86%） than in model group（P〈0.01）. Conclusion tISYA can inhibit protein nitration in brain ischemic injury, which may be one of the molecular mechanisms underlying the protection against cerebral ischemia/reperfusion injury.

关 键 词：脑缺血 脑梗死 再灌注损伤 羟基红花黄色素A 蛋白质硝基化 

分 类 号：R285.5[医药卫生—中药学]