# The effect of tert-butylhydroquinone on anxiolytic- and antidepressant-like behaviors induced by post-traumatic stress disorder: A behavioral and molecular study

## TL;DR

This study shows that tert-butylhydroquinone (tBHQ) can reduce anxiety and depression-like behaviors in rats with PTSD by affecting brain inflammation and stress-related proteins.

## Contribution

The study reveals a novel therapeutic potential of tBHQ in PTSD by linking its anti-inflammatory effects to behavioral and molecular changes in the brain.

## Key findings

- tBHQ reduced PTSD-induced anxiety and depression-like behaviors in rats.
- tBHQ counteracted PTSD-related increases in MAO-A, MAO-B, and IL-6, and decreases in IL-10 and glucocorticoid receptor.
- The effects were observed in the hippocampus and amygdala, key brain regions involved in stress and emotion.

## Abstract

Post-traumatic stress disorder (PTSD) is a crippling mental illness that commonly co-occurs with anxiety and depression. Recent studies have established a link between neuroinflammation and the development of PTSD. Studies have revealed that tert-butylhydroquinone (tBHQ) exhibits anti-inflammatory effects. This research investigated the impact of tBHQ on the amelioration of PTSD-induced depression- and anxiety-like behaviors with respect to amygdala and hippocampal MAO-A, MAO-B, IL-6, IL-10, and glucocorticoid receptor in rats.

PTSD was triggered through the use of Single Prolonged Stress (SPS). The Elevated Plus Maze (EPM) and Forced Swim Test (FST) were employed to evaluate anxiety and depression, respectively. Protein assessment utilized Western blot assay for IL-6, IL-10, and the glucocorticoid receptor, in addition to enzyme-linked immunosorbent assay (ELISA) for MAO-A and MAO-B.

The data demonstrated that treatment with tBHQ ameliorates the depression- and anxiety-like behaviors in rats with PTSD. The ELISA findings indicated a rise in both MAO-A and B proteins in the hippocampus and amygdala due to PTSD, which was counteracted by a subthreshold amount of tBHQ. Additionally, the Western blot assay techniques revealed that PTSD led to an elevation in IL-6 levels, a pro-inflammatory cytokine, and a reduction in IL-10 levels, along with a decrease in glucocorticoid receptor expression in both brain regions, which was also counteracted by a subthreshold amount of tBHQ.

These findings suggested that the beneficial effect of tBHQ on anxiety and depression induced by PTSD through hippocampal and amygdala MAO-A, MAO-B, IL-6, and IL-10, and glucocorticoid receptor.