The neurodegeneration, neuro-inflammation and mitochondrial dysfunction which happen by methamphetamine (METH) abuse or administration are significant and motivation therapeutic approaches for inhibition of these forms of neurodegeneration. As we know, METH by way of Toll-like receptors (TLRs), specially kind four, and NF-κB signaling pathway causes neuro-inflammation and mitochondrial dysfunction. Neuroprotective strategy for management of METH-induced neurodegeneration, inflammation and mitochondrial dysfunction, by way of a novel neuroprotective agent is constantly becoming superior to any type of other therapeutic approach. Hence, the clarification, introduction and improvement of efficacious novel neuroprotective agent are demanded. In the course of current years, utilizing new neuroprotective agent with therapeutic probability for therapy of METH-induced neuro-inflammation and mitochondrial dysfunction has been astoundingly elevated. Preceding research have stated the neuroprotective and anti-inflammatory roles ofcannabinoid derivate such as cannabidiol ( CBD) and delta-9-tetrahydrocannabinol (Δ9-THC) in several neurodegenerative events and illnesses. According to literature cannabinoid derivate, by inhibition of TLR4 and activation of NF-κB signaling pathway, exerts their anti-inflammatory and neuroprotective effects and lead to mitochondrial biogenesis. Hence we hypothesized that by utilizing cannabinoids in METH dependent topic it would deliver neuroprotection against METH-induced neurodegeneration, neuro-inflammation and mitochondrial dysfunction and in all probability can handle sequels of METH-induced neurochemical abuses by means of modulation of TLR4/NF-κB signaling pathway. In this post, we attempted to go over our hypothesis relating to the probable part of CBD and Δ9-THC, as a potent neuroprotective and anti-inflammatory agents, in inhibition or therapy of METH-induced neurodegeneration, neuro-inflammation and mitochondrial dysfunction by way of its effects on TLR4/NF-κB signaling pathway.
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