Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China ; Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China.
College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, 1 Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China.
Evid Based Complement Alternat Med. 2014;2014:383821. doi: 10.1155/2014/383821. Epub 2014 Apr 17.
The unregulated activation of microglia following stroke results in the production of toxic factors that propagate secondary neuronal injury. Salidroside has been shown to exhibit protective effects against neuronal death induced by different insults. However, the molecular mechanisms responsible for the anti-inflammatory activity of salidroside have not been elucidated clearly in microglia. In the present study, we investigated the molecular mechanism underlying inhibiting LPS-stimulated BV2 microglial cell mobility of salidroside. The protective effect of salidroside was investigated in microglial BV2 cell, subjected to stretch injury. Moreover, transwell migration assay demonstrated that salidroside significantly reduced cell motility. Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells. Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF- κ B) by blocking degradation of I κ B α and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression. These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.
中风后小胶质细胞的不受调节的激活导致产生了传播继发性神经元损伤的毒性因子。红景天苷已被证明对不同刺激诱导的神经元死亡具有保护作用。然而，红景天苷抗炎活性的分子机制在小胶质细胞中尚未阐明清楚。在本研究中，我们研究了红景天苷抑制 LPS 刺激的 BV2 小胶质细胞迁移的分子机制。研究了红景天苷在受拉伸损伤的小胶质细胞 BV2 中的保护作用。此外，Transwell 迁移实验表明，红景天苷可显著降低细胞迁移能力。我们的结果还表明，红景天苷以剂量依赖的方式抑制 LPS 诱导的趋化因子产生，而不会引起 BV2 小胶质细胞的细胞毒性。此外，红景天苷通过阻断 IκBα的降解和 MAPK（p38、JNK、ERK1/2）的磷酸化抑制 LPS 诱导的核因子κB（NF-κB）的激活，从而抑制趋化因子的表达。这些结果表明，红景天苷对 BV2 小胶质细胞的细胞迁移具有很强的抑制作用，这种化合物可能为伴有小胶质细胞激活的缺血性中风的治疗提供很大的治疗潜力。
