This study aims to assess the neuroprotective effect of AD4 against organophosphate-induced neurotoxicity. Experiments were conducted in a murine model that survives paraoxon exposure. Animals received either serum or AD4 as post-treatment therapy. Behavioral assessments were performed several days later to evaluate motor activity (HLA) and memory (NORT). Following euthanasia, proteins were extracted from distinct brain regions to analyze the expression of GPX, catalase, and lipid peroxidation marker 4-HNE. Additional animals were perfused, and brain sections were processed for immunohistochemical quantification of GFAP and IBA-1. The results demonstrate that AD4 26 mitigates oxidative stress, neuroinflammation, and cognitive dysfunction following acute paraoxon intoxication.

GraphPad Prism, 8.0

Western blot GPX1 in Hippocampus

Western blot GPX1 in Prefrontal Cortex

Western blot Catalasa in Hippocampus

Western blot Catalasa in Prefrontal Cortex

Quantification of 4-HNE adducts performed using a competitive ELISA kit, in Hippocampus

Quantification of 4-HNE adducts performed using a competitive ELISA kit, in Prefrontal Cortex

Immunofluorescence of GFAP in Dentate Gyrus of Hippocampus

Immunofluorescence of GFAP in CA1 of Hippocampus

Immunofluorescence of GFAP in CA3 of Hippocampus

Immunofluorescence of GFAP in Prefrontal Cortex

Immunofluorescence of IBA1 in Dentate Gyrus of Hippocampus

Raw data from immunofluorescence of IBA1 in CA1 of Hippocampus

Raw data from immunofluorescence of IBA1 in CA3 of Hippocampus

Raw data from the horizontal locomotor activity test

Raw data from time in every arm in the novel object recognition test