17β-trenbolone increases circulating myeloid-derived MMP8 in CSDS-induced mice and drives depressive tendencies to social threat.

Chronic psychosocial stress is a major risk factor for major depressive disorder (MDD). The impact of 17β-trenbolone (17-TB), an anabolic steroid and potential environmental endocrine disruptor, on stress responses and mood states in mammals is unclear. In this study, we explored how 17-TB interacts with chronic social defeat stress (CSDS) to drive neuroinflammatory cascades and behavioral abnormalities in mice.

17β-Trenbolone Increases the Release of Lipocalin 2 via the Brain-Liver Axis and Causes Alzheimer's Disease-Like Symptoms in CSDS-Induced Mice.

Aims: This study aimed to investigate the neurological and behavioural effects of exposure to the environmental endocrine disruptor 17β-trenbolone (17-TB) exposure in chronic social defeat stress (CSDS)-induced mice and elucidate the role of lipocalin 2 (LCN2) in linking peripheral inflammation to neurodegeneration.

Methods And Materials: Male BALB/c mice were subjected to the CSDS paradigm and treated with 17-TB (100 μg/kg) or vehicle control for 10 consecutive days. Behavioural assessments, including novel object recognition test, novel object location test and social interaction test, were conducted to evaluate cognitive memory and social behaviour.

17β-Trenbolone modulates anxiety-related synaptic plasticity by affecting the interaction between hippocampal TACR3 and systemic testosterone in male mice.

Anxiety Disorder is a common neurological disorder for which ubiquitous environmental endocrine disruptors may be risk factors. 17β-trenbolone (17-TB) has been recognized as a potential environmental endocrine disruptor and its neurotoxic effects have attracted attention. Tachykinin receptor 3 (TACR3), a G protein-coupled receptor involved in pubertal anxiety, and its underlying neural mechanisms remain enigmatic.