中文摘要：

目的 观察淫羊藿苷（ICA）对大脑中动脉阻塞诱导的缺血性脑卒中模型大鼠的保护作用,并探索其可能的作用机制.方法 雄性SD大鼠随机分为假手术组、模型组、ICA低、高剂量组及阳性药组（n=14）.ICA低、高剂量组每日两次灌胃ICA 10、30 mg＆#183;kg-1,阳性给药组每日灌胃尼莫地平10 mg＆#183;kg-1,连续给药1周,末次给药2h后采用右侧永久大脑中动脉阻塞（pMCAO）建立缺血性脑卒中模型.制模后继续给药.造模后24 h按Bederson法进行神经功能评分,TTC染色法测量脑梗死体积;HE染色观察缺血区组织的病理学变化;Real time RT-PCR测定梗死周围区TNF-α、IL-1β、COX-2及iNOS的mRNA表达;Western Blot检测梗死周围区COX-2和iNOS蛋白表达.结果 ICA明显降低了模型大鼠的神经功能评分,减少脑梗死体积,减轻缺血区组织的病理学损伤.同时,ICA明显抑制了pMCAO诱导的TNF-α、IL-1β、COX-2及iNOS的mRNA表达以及COX-2和iNOS的蛋白表达.结论 ICA对大鼠永久性脑缺血损伤有保护作用,其机制至少与抑制pMCAO后的炎症反应有关.

英文摘要：

Objective To investigate the effect of icafiin （ICA） on ischemic stroke induced by permanent mid- dle cerebral artery occlusion （pMCAO） in rats and explore the possible mechanisms. Methods Male Sprague Dawley rats were randomly divided into 5 groups ： sham, model, low - and high - dose of ICA - treated groups and positive group （n = 14）. Low- and high -dose ICA -treated groups were administered with ICA （10 and 30 mg· kg^-1 ） by gavage twice per day and the positive group was given nimodipine （ 10 mg· kg^-1 ）, while sham and model were treated with volume -matched distilled water. One week later,2 h after drug administra- tion, acute ischemic stroke was induced by fight permanent middle cerebral artery occlusion （pMCAO） in rats and then drug administration was continued. Twenty - four hours after model establishment, the neurological function was scored by the Bederson Test. Cerebral infarction volume was determined by 2,3,5 -triphenyhet- razolium chlorid （TYC） staining and the pathologic change in ischemic area was evaluated by H. E. staining. The mRNA expression of tumor necrosis factor alpha （ TNF - α） , interleukin - 1 beta （ IL - 1β）, cyclooxygen- ase - 2 （ COX - 2） and inducible nitric oxide synthase （iNOS） in peri - infarct region were detected by real time RT - PCR and the protein expression of COX - 2 and iNOS were also detected by Western Blot. Results ICA sig- nificantly caused a decrease in the change of neurological function and cerebral infarction volume, and attenuated the pathologic injury in pMCAO rats. Moreover, ICA prevented up - regulation of the mRNA expression of in- flammatory factors, including TNF -α, IL -β, COX - 2 and iNOS induced by pMCAO. The protein levels of COX -2 and iNOS were protective effect on acute dramatically decreased by pretreatment with ICA （30 mg/kg）. Conclusion ICA has the ischemie stroke in rats. The mechanisms are, at least partly, due to the inhibition of inflammatory responses following pMCAO.