he effects of vitamin B۱۲ on the brain damages caused by methamphetamine in mice

Objective(s): Methamphetamine (METH) is a powerful stimulant drug that directly affects the brain and induces neurological deficits. B۱۲ is a water-soluble vitamin (vit) that is reported to attenuate neuronal degeneration. The goal of the present study is to investigate the effect of vitamin B۱۲ on METH’s neurodegenerative changes.Materials and Methods: Two groups of ۶ animals received METH (۱۰ mg/kg, interaperitoneally (IP)) four times with a ۲ hr interval. Thirty mins before METH administration, vit B۱۲ (۱ mg/kg) or normal saline were injected IP. Animals were sacrificed ۳ days after the last administration. Caspase proteins levels were measured by Western blotting. Also, samples were examined by TUNEL assay to detect the presence of DNA fragmentation. Reduced glutathione (GSH) was also determined by the Ellman method.Results: The pathological findings showed that vit B۱۲ attenuates the gliosis induced by METH. Vit B۱۲ administration also significantly decreased the apoptotic index in the striatum and the cerebral cortex (P<۰.۰۰۱). It also reduced caspase markers compared to the control (PConclusion: The current study suggests that parenteral vit B۱۲ at safe doses may be a promising treatment for METH-induced brain damage via inhibition of  neuron apoptosis and increasing the reduced GSH level. Research focusing on the mechanisms involved in the protective responses of vit B۱۲ can be helpful in providing a novel therapeutic agent against METH-induced neurotoxicity.

کلیدواژه ها:

Cerebral cortex Methamphetamine Neurotoxicity ، Striatum ، Vitamin B۱۲