Ceftriaxone alleviates early brain injury after subarachnoid hemorrhage by increasing excitatory amino acid transporter 2 expression via the PI3K/Akt/NF-κB signaling pathway

FGF2 alleviates PTSD symptoms in rats by restoring GLAST function in astrocytes via the JAK/STAT pathway

“…Furthermore, AG490, a selective JAK/STAT inhibitor, decreases GLAST expression in vivo and in vitro, thus demonstrating that the JAK/STAT pathway is critical for the regulation of GLAST, but not GLT-1, in PTSD rats and in vitro primary astrocyte cultures; these results are similar to the findings for chronic perinatal hypoxia. Our previous study suggested that PI3K/AKT/ NF-κB signaling may be a potential mechanism of FGF2 regulating GLT-1 expression in astrocytes (Feng et al, 2014). Correlational analyses between NF-κB signaling and GLT-1 regulation in SPS-induced PTSD will be conducted in our future research.…”

“…The procedures for the glutamate analysis were the same as those of our previous study (Feng et al, 2014). Liquid CSF samples were collected from the cisterna magna.…”

Unravelling Pathophysiology of Crystalline Nephropathy in Ceftriaxone-Associated Acute Kidney Injury: A Cellular Proteomic Approach

“…In addition, further studies on the effects of “soluble” ceftriaxone on renal tubular cells would be of interest to better understand the pathophysiology of ceftriaxone-associated AKI. Note that the soluble ceftriaxone exhibited non-antimicrobial protective effects in models of neurological diseases, that is, Alexander’s disease [33, 34], Parkinson’s disease [35], and early brain injury after subarachnoid hemorrhage [36] and nephrotoxicity due to deltamethrin insecticide [37] and cadmium metal [38]. It is suspected that renal tubular cells would recognize and respond to soluble ceftriaxone and Cef-Ca crystals differently, and possession of this knowledge may have translational potentials in pediatric precision medicine.…”

GLT-1 transporter: An effective pharmacological target for various neurological disorders

“…GLT-1/EAAT-2 plays an integral role in both normal and abnormal neurotransmission (Guo et al, 2003). Beta-lactam-mediated activation of GLT-1/EAAT-2 expression is proposed to involve nuclear factor-kB (NF-kB), whereby β-lactams induce the nuclear activation of this transcription factor (Feng et al, 2014). Activated NF-kB then binds to the GLT-1/EAAT-2 promoter region and up-regulates the transcription of this gene (Lee et al, 2008), thereby decreasing glutamate concentration in the synaptic cleft and alleviating the potentially neurotoxic effects of excessive glutamate (Salles et al, 2014).…”