ArticleIranian journal of basic medical sciences2026
The effect of tert-butylhydroquinone on anxiolytic- and antidepressant-like behaviors induced by post-traumatic stress disorder: A behavioral and molecular study.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: 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. Materials and Methods: 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. Results: 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. Conclusion: 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.
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