Growth and neurotrophic factors have recently emerged as an important regulator of adult neurogenesis. Delivery of a neurotrophic factor can be a useful strategy for optimization of neurogenesis that improves the poor survival of newborn neurons. Acupuncture exerts therapeutic effects on animal models of pathologies through modulation of neurotrophin content in both the central nervous system and peripheral tissues. Our results showed that BDNF and VEGF mRNA levels were significantly increased by EA treatment among considerable six factors considered as important regulators of adult neurogenesis. BDNF and angiogenesis factor VEGF are two important neurotrophic factors that have multiple effects on neurogenesis. BDNF and VEGF stimulate adult neurogenesis and enhance the appearance and migration of new neurons in the SVZ and dentate gyrus. Post-ischemic intravenous BDNF treatment improves long-term functional neurological outcome for induction of neurogenesis. VEGF induces adult neurogenesis during exposure to an enriched environment or voluntary exercise and reduces apoptosis after its infusion, suggesting a survival promoting effect of NSCs. In examination of the brain by immunohistochemistry and Western blot, enhanced expression of mBDNF and VEGF occurred in parallel with the cellular proliferation and survival of NSCs. The current results imply potential roles of the BDNF and VEGF signaling pathway underlying the survival of NSCs. BDNF and VEGF mediate down-stream signaling cascades for survival of NSCs, such as PI3K/Akt or ERK pathways, via activation of the tyrosine kinase receptor and VEGF receptor 2, respectively. After the last session of EA, an increase in the number of pPI3K positive cells was detected in BrdU positive cells. In the current study, EA treatment improved neuronal function and induced proliferation and differentiation of NSCs through BDNF and VEGF signaling. The enhanced endogenous proliferation and maturation of NSCs in EA-treated mice may explain why functional recovery was observed after ischemic stroke. Consequently, EA stimulation induces proliferation of NSCs and promotes differentiation of proliferated cells into neurons or astrocytes, and provides the theoretical basis for a beneficial mechanism of EA treatment in post-ischemic stroke. Granulocyte colony-stimulating factor, also known as pluripoietin, controls the production, differentiation, and function of granulocytes, which account for 70% of white blood cells. The recruitment of two monomers of GCSF triggers Foretinib dimerization of the GCSF receptor and initiates a signaling cascade. Production of GCSF, which is secreted predominantly by macrophages, fibroblasts and endothelial cells, is stimulated by several inflammatory stimuli, including interleukin-1b, tumor necrosis factor-alpha, and lipopolysaccharide. Human GCSF has been approved for the treatment of neutropenia, a common disorder in cancer patients following radiotherapy or chemotherapy treatments, characterized by an extremely low number of neutrophils in the blood. GCSF also has neuroprotective properties.