Neuroprotective effects of vitamin B1 on memory impairment and suppression of pro-inflammatory cytokines in traumatic brain injury.

Abstract

Traumatic Brain Injury (TBI) remains one of the prevailing disorders that affect millions of people around the globe. There is a cascade of secondary attributes attached to TBI including excitotoxicity, axonal degeneration, neuroinflammation, oxidative stress, and apoptosis. Neuroinflammation is caused due to the activation of microglia along with pro-inflammatory cytokines. The activation of microglia triggers TNF-α which sequentially results in the triggering and upregulation of NF-kB. The aim of the current research was to investigate vitamin B1's potential as neuroprotective agent against TBI-induced neuroinflammation arbitrated memory impairment together with pre- and post-synaptic dysfunction in an adult albino male mice model. TBI was induced using the weight-drop method which caused the microglial activation resulting in neuroinflammation along with synaptic dysfunction leading to the memory impairment of the adult mice. Vitamin B1 was administered for seven days via the intraperitoneal pathway. To analyze the memory impairment and efficacy of vitamin B1, Morris water maze and Y-maze tests were performed. The escape latency time and short-term memories of the experimental mice treated with vitamin B1 were significantly different from the reference mice. The western blot results showed that vitamin B1 has reduced neuroinflammation by downregulating proinflammatory cytokines (NFκ-B, TNF- α). Vitamin B1 also proved its worthiness as a convincing neuroprotective agent by reducing memory dysfunction and recovering the activities of pre- and post-synapse via upregulation of synaptophysin and Postsynaptic density protein 95 (PSD-95).