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  • Sulfasalazine Some studies have demonstrated that


    Some studies have demonstrated that BMSCs can provide several trophic and growth factors that play important roles in cell survival, angiogenesis, and BMSC differentiation, but not cell replacement (Peled et al., 1999, Shen et al., 2007, Ji et al., 2004). This paracrine effect of BMSCs is a potential mechanism for angiogenesis and functional recovery after transplantation (Xu et al., 2013). Bakondi studies showed that human CD133-derived multipotent stromal Sulfasalazine (CD133dMSCs) secreted SDF-1 and protected mouse neural progenitor cell (mNPC) through CXCR7, so they thought SDF-1 is a key neuroprotective cytokine secreted by CD133dMSCs that protects mNPCs through CXCR7 (Bakondi et al., 2011). In agreement with those reports, we observed that SDF-1α expression was further increased in ischemic hippocampus after BMSC transplantation, and this was attenuated by treatment with AMD3100 or CXCR7 neutralizing antibody. These changes corresponded with the number of BMSCs that migrated to the ischemic hippocampus. Thus, we hypothesize that SDF-1α is released via a paracrine effect of BMSCs, and the increase in SDF-1α expression level further enhances BMSC homing to ischemic hippocampus.
    Experimental procedures
    Acknowledgments This work was supported by grants from the National Natural Science Foundation of China (No. 81171141) and the President Foundation of Xuzhou Medical College (No. 2010KJZ19).
    Introduction Depression can be perceived as a psychoneuroimmunological disorder in which cytokines affecting the body's neurochemical and neuroendocrine functions play an important role [1]. Cytokines are protein molecules affecting the growth, proliferation, and activation of the immune system and hematopoietic cells. They are responsible for signaling between cells of the immune system and have effects similar to hormones [2], [3]. Cytokines can affect the central nervous system function in several ways: by passing through a semi-permeable blood-brain barrier, by means of active transport through transport mechanisms specific for cytokines, and through activation of afferent nerve fibers, such as the vagus nerve, causing the transmission of stimuli to the appropriate regions of the brain, such as the nucleus of the solitary tract [4]. Among the cytokines, the effect of interleukin-6 (IL-6) on increased secretion of corticotropin-releasing hormone (CRH) is well described [5]. It is believed that the increased activity of the hypothalamic–pituitary–adrenal (HPA) axis is associated with the secretion of this hormone. The main disorder occurring in depression, which explains the increased activity of the HPA axis, is the weakening of its inhibitory mechanism. The increase in corticosteroid concentration that occurs in chronic stress can exacerbate depression [6]. Cytokines, which are intracellular polypeptides, are involved in transmitting information from the immune system to the brain and the neuroendocrine system. Cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-α (TNF-α) have the ability to directly stimulate the HPA axis and release corticotropin-releasinghormone (CRH) [7]. Furthermore, numerous studies involving patients have shown that antidepressants reduce the concentration of IL-6 [8], [9]. On the other hand, there are fewer studies on the role of chemotactic cytokines (chemokines) in depression [10], [11], [12]. In a study on mice and rats, Haroon et al. [13] described the participation of chemokines: monocyte chemotactic protein-1 (MCP-1), chemokine (C-X3-C motif) ligand-1 (CX3CL1; fractalkine), as well as chemokine receptors: CX3C chemokine receptor-1 (CX3CR1; fractalkine receptor), C-C chemokine receptor type 5 (CCR5) and chemokine (C-X-C motif) receptor-4 (CXCR4) in the formation of behavior resembling depression (depressive-like behavior). The authors stressed that the increase in the level of proinflammatory chemokine and the activation of their receptors may contribute to the intensity of inflammation and the severity of depression.