Salt (sodium chloride, NaCl) accumulation in the brain is associated with various diseases of central nervous system (CNS). Activation of astrocytes is an important manifestation of pathophysiological processes in the CNS. However, the direct impact of high salt (HS) environment on astrocytes is unclear. In the current study, we found that high salt treatment can induce activation of astrocytes both in vivo and in vitro, manifested as morphological alteration coupled with increased expression of glial fibrillary acidic protein (GFAP). Additionally, HS upregulated the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and vascular endothelial growth factor (VEGF); however, its effects on transforming growth factor-β (TGF-β) expression were not evident. Furthermore, HS treatment induced increased phosphorylation of signal transducer and activator transcription 3 (STAT 3). Inhibition of Janus kinase 2 (JAK 2) by specific pharmacological antagonists, AG490, attenuated the activation of JAK2/STAT3 pathway and induction of GFAP and other pro-inflammatory factors, respectively. The results suggest that the aforementioned multiple inflammatory cytokines and mediators that may be linked to the HS induced pathogenesis of CNS via the JAK2/STAT3 signaling pathways.
Keywords: astrocytes; inflammatory cytokines; salt.