Stroke is the leading cause of long-term motor disability and cognitive impairment beside the acute brain injury. Recently, neurogenesis has become an attractive strategy for the chronic recovery of stroke. Our previous study showed that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, isolated from leaves of Panax pseudoginseng subsp., exerted neuroprotective effects on stroke by alleviating autophagy/lysosomal defects and repressing calcium overload. The present study investigated whether PF11 improved long-term functional recovery and promoted neurogenesis after ischemic stroke induced by transient middle cerebral artery occlusion (tMCAO) in mice. The data showed that PF11 (16, 32 mg/kg, p.o.) administrated once daily one week before tMCAO significantly reduced brain infarction and brain edema on day 3 after tMCAO. Also, PF11 attenuated the mortality, sensorimotor dysfunction, cognitive impairment and hippocampal atrophy of stroke mice. Moreover, the migration of neuroblasts and the generation of newborn neurons in ipsilateral striatum and dentate gyrus (DG) were significantly enhanced by PF11. In line with this, PF11 prevented the decreased survival rate of newborn neurons on day 42 after tMCAO. In addition, PF11 promoted proliferation and differentiation of neural stem cells in vitro. Furthermore, PF11's pro-neurogenic effect was attributed to its activation of the BDNF/TrkB, which was evidenced by that the pharmacological effects of PF11 was abolished by ANA-12, a specific inhibitor of BDNF receptor. Thus, the present study showed that PF11 could improve long-term neurological impairment and promote neurogenesis after stroke possibly through activating BDNF/TrkB pathway, indicating its potential role on treating ischemic stroke, especially chronic recovery.

中文翻译：

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Pseudoginsenoside-F11可改善小鼠短暂性脑缺血后的长期神经功能，并促进神经发生。

除急性脑损伤外，中风是长期运动障碍和认知障碍的主要原因。最近，神经发生已成为中风的慢性恢复的有吸引力的策略。我们先前的研究表明，从人参亚种叶中分离出的一种人参皂甙F11假人参皂苷F11通过减轻自噬/溶酶体缺陷和抑制钙超载，对中风发挥了神经保护作用。本研究调查了PF11是否改善了小鼠短暂中脑动脉闭塞（tMCAO）诱发的缺血性中风后的长期功能恢复并促进了神经发生。数据显示，在tMCAO之前的一周内每天一次给药PF11（16，32 mg / kg，口服），在tMCAO后的第3天可显着减少脑梗塞和脑水肿。还，PF11可减轻中风小鼠的死亡率，感觉运动功能障碍，认知障碍和海马萎缩。此外，PF11显着增强了同侧纹状体和齿状回（DG）中成神经细胞的迁移和新生神经元的生成。与此相符，PF11预防了tMCAO后第42天新生神经元的存活率降低。另外，PF11在体外促进神经干细胞的增殖和分化。此外，PF11的促神经源性作用归因于其对BDNF / TrkB的激活，这可以通过BD-12受体的特异性抑制剂ANA-12消除PF11的药理作用来证明。因此，