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目的:探讨黄芩茎叶总黄酮(scutellaria baicalensis stem-leave total flavonoid,SSTF)预处理对局灶性脑缺血再灌注(I/R)大鼠海马的保护作用及其机制。方法:60只SD大鼠随机分为3组,假手术组、缺血再灌注组和SSTF预处理组。SSTF预处理组术前1周给予SSTF 100 mg.kg-1.d-1,其余两组给等量PBS。各组大鼠分别灌胃给药1周后,采用线栓法制备局灶性脑缺血再灌注模型,缺血2 h再灌注24 h后观察海马区病理形态学改变及神经元密度,检测海马Fas,FasL蛋白的表达和海马组织中谷胱甘肽过氧化物酶(GSH-Px)活性、丙二醛(MDA)含量及乳酸脱氢酶(LDH)活性的改变。结果:SSTF预处理可减轻损伤海马组织的病理学改变,使存活的神经元增加(180±13.2)。与I/R组比较,SSTF预处理组海马Fas,FasL阳性细胞明显减少(分别为13.26±3.18,19.08±2.76)。SSTF预处理可降低缺血再灌注引起的海马组织MDA含量增加(P<0.05),提高GSH-Px,LDH酶活性(P<0.01)。结论:SSTF预处理对I/R损伤海马具有保护作用。其作用机制可能与下调Fas,FasL表达和提高I/R大鼠海马组织抗氧化能力有关。
Objective: To investigate the protective effects of scutellaria baicalensis stem-leave total flavonoid (SSTF) on the hippocampus of focal cerebral ischemia-reperfusion (I / R) rats and its mechanism. Methods: Sixty SD rats were randomly divided into three groups: sham operation group, ischemia reperfusion group and SSTF pretreatment group. The SSTF pretreatment group was given SSTF 100 mg.kg-1.d-1 one week before operation and the other two groups were given the same amount of PBS. One week after intragastric administration, rats in each group were given focal cerebral ischemia / reperfusion model by thread embolization method. Pathological changes and neuron density in hippocampus were observed 24 hours after reperfusion for 2 hours. The expressions of Fas and FasL in hippocampus and the activity of glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and activity of lactate dehydrogenase (LDH) in hippocampus were detected. Results: SSTF pretreatment could reduce the pathological changes of injured hippocampal tissue and increase the number of viable neurons (180 ± 13.2). Compared with I / R group, Fas and FasL positive cells in hippocampus of SSTF preconditioning group were significantly decreased (13.26 ± 3.18 and 19.08 ± 2.76, respectively). SSTF pretreatment could decrease the MDA content in hippocampus (P <0.05) and increase the activity of GSH-Px and LDH (P <0.01). Conclusion: Pretreatment with SSTF can protect hippocampus of I / R injury. Its mechanism may be related to down-regulating the expression of Fas and FasL and enhancing the anti-oxidation ability of hippocampus in I / R rats.