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目的研究sparstolonin B(8,5’-dihydroxy-4-phenyl-5,2’-oxidoisocoumarin,Ssn B)对脑出血(intracerebral haemorrhage,ICH)诱导的大鼠脑损伤的保护作用。方法体外Transwell实验观察Ssn B对血红蛋白(hemoglobin,Hb)诱导的小胶质细胞损伤神经元的影响;采用自体血注射脑出血模型,出血后的第1、3、5、7天观察Ssn B对ICH大鼠神经功能缺损评分(neurological deficit score,NDS),脑组织含水量的影响,ELISA法检测ICH大鼠脑组织匀浆中炎性细胞因子白细胞介素(IL)-6、IL-1β和肿瘤坏死因子(TNF)-α的含量变化。结果第1、3天,5和15 mg·kg~(-1)Ssn B都能减少ICH大鼠的NDS,降低ICH大鼠脑组织含水量,明显下调脑血肿周围组织中炎性细胞因子的含量。结论 Ssn B对ICH大鼠脑损伤有保护作用,其机制可能与Ssn B保护受损神经元,减轻脑出血大鼠神经功能缺损,降低脑组织含水量和炎症因子有关。
Objective To investigate the protective effect of sparstolonin B (8,5’-dihydroxy-4-phenyl-5,2’-oxidoisocoumarin, Ssn B) on brain injury induced by intracerebral haemorrhage (ICH) in rats. Methods The effects of Ssn B on hemoglobin (Hb) -induced microglial neurons were observed by Transwell assay in vitro. Autologous blood was injected into the intracerebral hemorrhage model to observe the Ssn B ICH rat neurological deficit score (NDS), water content of brain tissue, and the levels of inflammatory cytokines IL-6, IL-1β Tumor necrosis factor (TNF) -α content changes. Results Ssn B at 5 and 15 mg · kg -1 could reduce the NDS of ICH rats on day 1, day 3, decrease the water content in brain of ICH rats and obviously down-regulate the expression of inflammatory cytokines content. Conclusion Ssn B can protect brain injury of ICH rats. Its mechanism may be related to the protection of injured neurons by Ssn B, the neurological deficits and the decrease of brain water content and inflammatory cytokines in ICH rats.