Betaine prevents homocysteine-induced memory impairment via matrix metalloproteinase-9 in the frontal cortex.

摘要: Abstract Betaine plays important roles that include acting as a methyl donor and converting homocysteine (Hcy) to methionine. Elevated plasma Hcy levels are known hyperhomocysteinemia (HHcy) contribute impairments of learning memory. Although it is commonly betaine an role in metabolism, the effects on Hcy-induced memory impairment have not been investigated. Previously, we demonstrated beneficial acute stress lipopolysaccharide-induced impairment. In present study, investigated whether ameliorates underlying mechanisms this putative effect. Mice were treated with (0.162 mg/kg, s.c.) twice day for nine days, (25 mg/kg, was administered 30 min before injections. The functions evaluated using spontaneous alternation performance test (Y-maze) at seven days step-down type passive avoidance (SD) ten after injection. We found suppressed induced by repeated However, blood concentrations significantly increased Hcy-treated mice immediately test, did prevent increase. Furthermore, induces redox part activating matrix metalloproteinase-9 (MMP-9), which leads BBB dysfunction. Therefore, tested affected MMP-9 activity. Interestingly, treatment inhibited activity frontal cortex but hippocampus These results suggest changes might partially responsible amelioration deficits be candidate therapeutic target HHcy.