摘要
目的观察三七皂甙Rb1对缺氧缺血新生大鼠脑梗死体积、内源性一氧化碳(CO)水平及血红素加氧酶-1(HO-1)表达的影响,探讨三七皂甙Rb1抗脑缺血损伤作用及其可能的分子机制。方法 7日龄新生SD大鼠建立缺氧缺血性脑损伤(HIBD)动物模型,将动物随机分为4组:9 g.L-1盐水组,2 mg.kg-1三七皂甙Rb1组(低剂量组)、10 mg.kg-1三七皂甙Rb1组(中剂量组)、50 mg.kg-1三七皂甙Rb1组(高剂量组)。各组大鼠分别腹腔注射9 g.L-1盐水和不同剂量三七皂甙Rb1。心脏取血,检测全血碳氧血红蛋白(COHb)水平。检测其海马组织HO-1活性变化,采用反转录-PCR检测其海马HO-1 mRNA的表达。结果低剂量组、中剂量组、高剂量组与9 g.L-1盐水组比较,脑缺氧缺血后脑梗死体积显著减少。中剂量组与高剂量组、低剂量组相比,脑缺氧缺血后全血COHb水平显著升高,海马HO-1活性显著增加(Pa<0.05)。中剂量组大鼠海马HO-1 mRNA的表达水平明显高于其他各组(Pa<0.05)。结论三七皂甙Rb1可能通过增加COHb水平和脑局部HO-1活性改善缺氧缺血脑损伤。三七皂甙Rb1在脑缺氧缺血中的脑保护作用可能与增强脑局部HO-1 mRNA表达有关。
Objective To observe the volume of cerebral infarction and the expression of heme oxygenase 1（HO-1） and the content of carbon monoxide（CO） in neonatal rats with cerebral hypoxic-ischemia,and investigate the possible molecular mechanism of neuroprotective effects of arasaponin Rb1.Methods Neonatal SD rats,aged seven-day-old,were divided randomly into 4 groups：normal saline group,2 mg·kg^-1arasaponin Rb1 group（low dose group）,10 mg·kg^-1arasaponin Rb1 group（meddle dose group） and 50 mg·kg^-1arasaponin Rb1 group（high dose group） after hypoxic-ischemic brain damage models were established.The changes of HO-1 mRNA in hippocampus were assessed by the reverse transcriptase-polymerase chain reaction（RT-PCR）,and blood carbonyl haemoglobin（COHb） and variation of HO-1 activity in hippocampus were determined.Results Administration of meddle dose of arasaponin Rb1 greatly diminished the volume of cerebral infarction.Administration of meddle dose of arasaponin Rb1 greatly increased the content of COHb and activity of HO-1 in hippocampus（Pa〈0.05）.Administration of meddle dose of arasaponin Rb1 also greatly increased the expression of HO-1 mRNA（P〈0.05）.Conclusions Arasaponin Rb1 ameliorates the cerebral damage and diminishes the volume of cerebral infarction by escalating the contents of COHb and activity of HO-1 in hippocampus.Furthermore,the protective effect of arasaponin Rb1 has relationship with enhancing the expression of HO-1 mRNA.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2010年第18期1422-1424,共3页
Journal of Applied Clinical Pediatrics
基金
河南省教育厅自然科学研究计划项目(2008B180012)
作者简介
李彦，女，讲师，硕士学位，研究方向为缺血再灌注损伤，电子信箱drleeyan@163．com。
通讯作者：李炳，男，讲师，博士生，研究方向为脑损伤的病理机制，电子信箱libing22@126．com。
