Zhuang Pengwei, Wan Yanjun, Geng Shihan, He Ying, Feng Bo, Ye Zhengliang, Zhou Dazheng, Li Dekun, Wei Hongjun, Li Hongyan, Zhang Yanjun, Ju Aichun
Chinese Materia Medica College, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China; Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China; Tianjin JF-Pharmaland Technology Development Co., Ltd., Tianjin, China.
Chinese Materia Medica College, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China; Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
J Ethnopharmacol. 2017 Feb 23;198:194-204. doi: 10.1016/j.jep.2016.11.052. Epub 2017 Jan 10.
Inflammatory reactions induced by microglia in the brain play crucial roles in ischemia/reperfusion (I/R) cerebral injuries. Microglia activation has been shown to be closely related to TLR4/NF-κB signal pathways. Salvianolic acids for injection (SAFI) have been used in clinical practice to treat ischemic stroke with reported neuroprotective effects; however, the underlying mechanisms are still uncertain.
First, we studied the effect of SAFI on inflammatory responses in LPS-stimulated BV-2 microglia. Then, to discover whether the beneficial in vitro effects of SAFI lead to in vivo therapeutic effects, an MCAO (Middle cerebral artery occlusion) rat model was further employed to elucidate the probable mechanism of SAFI in treating ischemic stroke. Rats in the SAFI group were given SAFI (23 or 46mg/kg) before I/R injury.
The results showed that SAFI treatment significantly decreased neuroinflammation and the infarction volume compared with the vehicle group. Activation of microglia cells was reduced, and TLR4/NF-κB signals, which were markedly inhibited by SAFI treatment in ischemic hemisphere, were accompanied by reduced expression and release of cytokines IL-1β and IL-6.
This study provides evidence that SAFI effectively protects the brain after cerebral ischemia, which may be caused by attenuating inflammation in microglia.
脑内小胶质细胞诱导的炎症反应在缺血/再灌注（I/R）脑损伤中起关键作用。小胶质细胞激活已被证明与TLR4/NF-κB信号通路密切相关。注射用丹参酸（SAFI）已在临床实践中用于治疗缺血性中风，据报道具有神经保护作用；然而，其潜在机制仍不确定。
首先，我们研究了SAFI对脂多糖刺激的BV-2小胶质细胞炎症反应的影响。然后，为了探究SAFI在体外的有益作用是否能产生体内治疗效果，进一步采用大脑中动脉闭塞（MCAO）大鼠模型来阐明SAFI治疗缺血性中风的可能机制。SAFI组大鼠在I/R损伤前给予SAFI（23或46mg/kg）。
结果表明，与载体组相比，SAFI治疗显著降低了神经炎症和梗死体积。小胶质细胞的激活减少，SAFI治疗在缺血半球显著抑制的TLR4/NF-κB信号伴随着细胞因子IL-1β和IL-6表达和释放的减少。
本研究提供了证据表明SAFI能有效保护脑缺血后的大脑，这可能是由于减轻了小胶质细胞中的炎症所致。
