Wang Xinying, Yang Guofeng
Department of Neurology, Hebei Medical University, No. 361, East Zhongshan Road, Shijiazhuang 050017, Hebei, China; Department of Neurology, Harrison International Peace Hospital, No.180, East Renmin Road, Hengshui 053000, Hebei, China.
Department of Geriatrics, Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang 050000, Hebei, China.
Transl Neurosci. 2020 Jul 2;11(1):227-235. doi: 10.1515/tnsci-2020-0129. eCollection 2020.
Inflammation is involved in cerebral ischemia/reperfusion (I/R)-induced neurological damage. Saikosaponin A (SSa), extracted from , has been reported to exert anti-inflammatory effects. This article aimed to investigate whether SSa could ameliorate neuroinflammation mediated by ischemic stroke and the underlying mechanism.
Rat middle cerebral artery occlusion (MCAO) model was employed in this study, and the cognitive and motor functions were detected by behavioral tests. Inflammatory cytokines in the serum were detected by ELISA kits. The expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and high-mobility group box 1 (HMGB1) in the brain tissues were assayed with Western blot.
Our results showed that SSa pretreatment could significantly reduce brain damage, improve neurological function recovery, and decrease the water content of brain tissues when compared with the model group. SSa pretreatment significantly reduced the serum HMGB1 level and downregulated the contents of inflammatory cytokines including tumor necrosis factor-α, interleukin-1 beta, and interleukin-6. Furthermore, SSa pretreatment could attenuate the decreased TLR4 and nucleus NF-κB in the brain of MCAO rats. The protein level of HMGB1 in the nucleus was significantly upregulated in the SSa pretreatment group.
Our results suggested that the pretreatment with SSa provided significant protection against cerebral I/R injury in rats via its anti-inflammation property by inhibiting the nucleus HMGB1 release.
炎症参与了脑缺血/再灌注(I/R)诱导的神经损伤。从柴胡中提取的柴胡皂苷A(SSa)已被报道具有抗炎作用。本文旨在研究SSa是否能改善缺血性中风介导的神经炎症及其潜在机制。
本研究采用大鼠大脑中动脉闭塞(MCAO)模型,通过行为测试检测认知和运动功能。用ELISA试剂盒检测血清中的炎性细胞因子。用蛋白质印迹法检测脑组织中Toll样受体4(TLR4)、核因子-κB(NF-κB)和高迁移率族蛋白B1(HMGB1)的表达水平。
我们的结果表明,与模型组相比,SSa预处理可显著减少脑损伤,改善神经功能恢复,并降低脑组织含水量。SSa预处理显著降低血清HMGB1水平,并下调包括肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6在内的炎性细胞因子含量。此外,SSa预处理可减轻MCAO大鼠脑中TLR4和核NF-κB的降低。SSa预处理组细胞核中HMGB1的蛋白水平显著上调。
我们的结果表明,SSa预处理通过抑制细胞核HMGB1释放,发挥抗炎特性,对大鼠脑I/R损伤提供了显著保护。