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Vitamin C (ascorbic acid: AA) uptake in neurons occurs via the sodium-dependent vitamin C transporter-2 (SVCT2), which is highly expressed in the central nervous system (CNS). During chronic neuroinflammation or infection, CNS levels of lipopolysaccharide (LPS) and LPS-induced tumor necrosis factor- α  (TNF α ) are increased. Elevated levels of LPS and TNF α  have been associated with neurodegenerative diseases together with reduced levels of AA. However, little is known about the impacts of LPS and TNF α  on neuronal AA uptake. The objective of this study was to examine the effect of LPS and TNF α  on SVCT2 expression and function using  in vitro  and  in vivo  approaches. Treatment of SH-SY5Y cells with either LPS or TNF α  inhibited AA uptake. This reduced uptake was associated with a significant decrease in SVCT2 protein and mRNA levels.  In vivo  exposure to LPS or TNF α  also decreased SVCT2 protein and mRNA levels in mouse brains. Both LPS and TNF α  decreased  SLC23A2  promoter activity. Further, the inhibitory effect of LPS on a minimal  SLC23A2  promoter was attenuated when either the binding site for the transcription factor Sp1 was mutated or cells were treated with the NF- κ B inhibitor, celastrol. We conclude that inflammatory signals suppress AA uptake by impairing  SLC23A2  transcription through opposing regulation of Sp1 and NF- κ B factors.

Effect of Lipopolysaccharide and TNFα on Neuronal Ascorbic Acid Uptake