Amelioration of Radiation-Induced Cell Death in Neuro2a Cells by Neutralizing Oxidative Stress and Reducing Mitochondrial Dysfunction Using N-Acetyl-L-Tryptophan

Figure 12

A summarized diagrammatic illustration to demonstrate the possible role of L-NAT in radioprotection. L-NAT binds with NK-1R and inhibits Substance P binding with its preferred receptor, i.e., NK-1R. The interaction of L-NAT with the NK-1R cellular system may be activated to maintain oxidative stress by reducing ROS, enhancing antioxidant enzymes activity, mitochondrial redox homeostasis, inhibit accumulation of Ca²⁺ ion concentration in the mitochondrial matrix, inhibiting apoptosis via inhibition of caspase-3 and γ-H2aX expression, as well as an increase in p53 and p-EKR1/2 expression that may contribute to achieving the desired level of radioprotection in Neuro2a cells.^{# #}we use http://BioRender.com for creating these Diagrams.