Abstract
BackgroundBetaine (glycine betaine or trimethylglycine) plays important roles as an osmolyte and a methyl donor in animals. While betaine is reported to suppress expression of proinflammatory molecules and reduce oxidative stress in aged rat kidney, the effects of betaine on the central nervous system are not well known. In this study, we investigated the effects of betaine on lipopolysaccharide (LPS)-induced memory impairment and on mRNA expression levels of proinflammatory molecules, glial markers, and GABA transporter 2 (GAT2), a betaine/GABA transporter.MethodsMice were continuously treated with betaine for 13 days starting 1 day before they were injected with LPS, or received subacute or acute administration of betaine shortly before or after LPS injection. Then, their memory function was evaluated using Y-maze and novel object recognition tests 7 and 10-12 days after LPS injection (30 μg/mouse, i.c.v.), respectively. In addition, mRNA expression levels in hippocampus were measured by real-time RT-PCR at different time points.ResultsRepeated administration of betaine (0.163 mmol/kg, s.c.) prevented LPS-induced memory impairment. GAT2 mRNA levels were significantly increased in hippocampus 24 hr after LPS injection, and administration of betaine blocked this increase. However, betaine did not affect LPS-induced increases in levels of mRNA related to inflammatory responses. Both subacute administration (1 hr before, and 1 and 24 hr after LPS injection) and acute administration (1 hr after LPS injection) of betaine also prevented LPS-induced memory impairment in the Y-maze test.ConclusionsThese data suggest that betaine has protective effects against LPS-induced memory impairment and that prevention of LPS-induced changes in GAT2 mRNA expression is crucial to this ameliorating effect.
Highlights
Betaine plays important roles as an osmolyte and a methyl donor in animals
We investigated whether repeated administration of betaine could prevent LPS-induced increases in mRNA expression levels for proinflammatory molecules such as IL-1b, tumor necrosis factor (TNF)-a, inducible nitric oxide synthase (iNOS), and COX2
Betaine may act on GABA transporter 2 (GAT2)/Betaine/GABA transporter-1 (BGT-1) expressed in neurons and/or glial cells to improve memory impairment; we examined the effects of LPS and betaine iNOS / ß-actin (C)
Summary
Betaine (glycine betaine or trimethylglycine) plays important roles as an osmolyte and a methyl donor in animals. While betaine is reported to suppress expression of proinflammatory molecules and reduce oxidative stress in aged rat kidney, the effects of betaine on the central nervous system are not well known. Dietary betaine suppresses the activation of nuclear factor-B (NF-B) with oxidative stress, and the protein expression of proinflammatory molecules such as cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and tumor necrosis factor (TNF)-a in aged rat kidneys [6,7]. Since GAT2 is co-localized with Pglycoprotein, a blood-brain barrier (BBB)-specific marker, in brain capillaries [12], it may be involved in betaine transport across the BBB These data suggest that betaine attenuates inflammatory processes and/or oxidative stress; the effects of betaine on central nervous system function in animals are poorly understood
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