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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·kg-1,阳性给药组每日灌胃尼莫地平10 mg·kg-1,连续给药1周,末次给药2 h后采用右侧永久大脑中动脉阻塞(p MCAO)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i NOS的mRNA表达;Western Blot检测梗死周围区COX-2和i NOS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p MCAO诱导的TNF-α、IL-1β、COX-2及i NOS的mRNA表达以及COX-2和i NOS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p MCAO后的炎症反应有关。
Objective To observe the protective effect of icariin (ICA) on the middle cerebral artery occlusion-induced ischemic stroke model rats and to explore its possible mechanism. Methods Male Sprague-Dawley rats were randomly divided into sham operation group, model group, ICA low, high dose group and positive drug group (n = 14). ICA low and high dose groups were given intragastrically ICA 10,30 mg · kg-1 twice a day, while the positive group was given nimodipine 10 mg · kg-1 daily for 1 week and the last dose 2 h after the right side of the middle cerebral artery occlusion (p MCAO) to establish the ischemic stroke model. Formulation continue to give medicine. Neurological function scores were measured by Bederson method at 24 h after modeling. The volume of cerebral infarction was measured by TTC staining. The pathological changes of ischemic tissue were observed by HE staining. The levels of TNF-α, IL-1β, COX-2 and iNOS mRNA expression; Western Blot detection infarct peripheral COX-2 and iNOS protein expression. Results ICA significantly reduced the neurological function score of model rats, decreased the volume of cerebral infarction, and alleviated the pathological damage of ischemic tissues. Meanwhile, ICA significantly inhibited p MCAO-induced mRNA expression of TNF-α, IL-1β, COX-2 and iNOS as well as COX-2 and iNOS protein expression. Conclusion ICA has a protective effect on permanent cerebral ischemia injury in rats, and its mechanism is at least related to inhibition of inflammatory reaction after p MCAO.