Abstract
Increased Hcy has a toxic effect on nerve cells and can cause hippocampal death and directly damage the body’s cognitive function and memory ability, leading to the occurrence of vascular dementia. Hcy predicts vascular disease and might be a basis for clinical judgment. This article provides a new basis for the prevention and treatment of this disease by exploring the mechanism of action of memantine hydrochloride in diabetic vascular dementia. After grouping, mice walked through the Morris water maze to record the escape latency, and measured the Hcy level of the mice by high performance liquid chromatography. Observing the volume of brain atrophy in mice. GFAPT, APP, and CHAT level in mouse hippocampus was assessed by IHC and CHAT mRNA was detected by RT-PCR. Escape latency, Hcy level (11.46 ±0.74) yiimmol/L, brain atrophy volume (25.21 ±1.21) mm3, number of APP positive cells (46.7003±3.2431), number of GFAP positive cells (21.4000 ± 1.8127) were all significantly lower than those of model group. The positive rate of CHAT and the amount of CHAT mRNA in the memantine hydrochloride group was significantly elevated (P < 0.05) with higher CHAT mRNA than model group and lower than blank group (P < 0.05). Memantine hydrochloride could reduce the level of Hcy in mice, improve the cognitive function of mice with diabetic vascular dementia by improving the number of GFAP and CHAT positive cells in hippocampus and cortex, and increasing the amount of CHAT mRNA in brain tissue.
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