【摘要】 目的观察淫羊藿苷(ICA)对大鼠脑缺血-再灌注损伤的保护作用并探讨其机制。方法 SD大鼠40只,随机分为假手术组、模型组、ICA低剂量组(30 mg/kg)和ICA高剂量组(80 mg/kg),每组10只。造模前假手术组、模型组予同体积0.9%氯化钠注射液,ICA高、低剂量组分别腹腔注射80、30 mg/kg剂量的ICA 2 m L。给药7 d后,采用颈总动脉夹闭法制备脑缺血-再灌注损伤模型。缺血0.5 h后,再灌注24 h分别检测缺血脑组织谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、髓过氧化物酶(MPO)活性、一氧化氮(NO)含量和一氧化氮合酶(NOS)活性;采用酶联免疫吸附测定(ELISA)法检测脑组织肿瘤坏死因子-α(TNF-α)和血清白细胞介素-1β(IL-1β)的含量。结果脑缺血-再灌注24 h后与假手术组比较,模型组GSH-Px、SOD活性值差异有统计学意义(P <0.01);与模型组比较,ICA低剂量组和ICA高剂量组大鼠脑组织GSH-Px、SOD活性明显增高,差异有统计学意义(均P <0.01)。与假手术组比较,模型组MDA含量、MPO活性、NO含量、NOS活性、TNF-α含量、血清IL-1β含量差异有统计学意义(P <0.01);与模型组比较,ICA低剂量组和ICA高剂量组大鼠脑组织MDA含量、MPO活性、NO含量、NOS活性、TNF-α含量、血清IL-1β含量明显减低,差异有统计学意义(均P <0.01)。结论 ICA对大鼠脑缺血-再灌注损伤具有神经保护作用,其机制可能与增高GSH-Px、SOD活性、降低MDA含量,抑制自由基损伤;降低NO含量、NOS活性,抑制神经毒性损伤;降低MPO活性、TNF-α、IL-1β含量抑制炎症反应损伤有关。更多还原

【Abstract】 Objective: To explore the protective effects and mechanism of Icariin on cerebral ischemia-reperfusion injury in rats. Methods: 40 SD rats were divided into the sham operation group,the model group,Icariin low-dose group,Icariin high-dose group. Cerebral ischemia-reperfusion model was established with carotid artery clamping method. GSH-Px activity,SOD activity and MDA contents,MPO activity,NO contents,NOS activity were measured in the 24 th hour after the cerebral reperfusion post 0.5 h ischemia. The contents of TNF-α and IL-1β were detected by ELISA. Results: In the 24 th hour after the cerebral ischemia-reperfusion,compared with the sham operation group,the model group had significant difference in GSH-Px and SOD activity,MDA content,MPO activity,NO content,NOS activity,TNF-α content and serum IL-1β content(P < 0.01). Compared with the model group,the activity of GSH-Px and SOD increased significantly,and MDA content,MPO activity,NO content,NOS activity,TNF-α content and serum IL-1β content decreased significantly in ICA groups,with significant difference(P < 0.01). Conclusion: ICA has neuroprotective effect on cerebral ischemia-reperfusion injury in rats.Its mechanism may be related to increasing GSH-Px and SOD activity,decreasing MDA content,inhibiting free radical damage,reducing NO content and NOS activity,inhibiting neurotoxic damage,reducing MPO activity and the contents of TNF-α and IL-1β,and inhibiting inflammation damage.更多还原