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<p>Chronic glucocorticoid therapy, while clinically indispensable, often induces debilitating neuropsychiatric side effects, including depression-like behaviors, alongside systemic immunosuppression and metabolic dysfunction. The convergence of central neurotoxicity and peripheral immune dysregulation presents a unique therapeutic challenge requiring multi-target interventions. This study investigated the prophylactic efficacy of lycopene against dexamethasone-induced behavioral, neurochemical, oxidative, inflammatory, and immunological perturbations in rats. Thirty-two adult male Sprague-Dawley rats were randomly assigned to four groups (<i>n</i> = 8): normal control, dexamethasone (2&#xa0;mg/kg/day/intraperitoneal), lycopene (10&#xa0;mg/kg/day/orally), and dexamethasone+lycopene combination. Treatments were administered daily for 21 days. Behavioral assessments (forced swim test, tail suspension test) were conducted. In frontal cortex and hippocampal tissues, neurochemical markers (brain-derived neurotrophic factor, gamma-aminobutyric acid, and acetylcholinesterase activity), neurotransmitters (serotonin, dopamine), oxidative stress markers (malondialdehyde, nitric oxide, reduced glutathione, superoxide dismutase, catalase), inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6), and caspase-3 were quantified. In serum, fasting blood glucose, insulin, liver and kidney function markers, oxidative stress markers, inflammatory cytokines (interleukin-4, tumor necrosis factor-alpha, interferon-gamma), cluster of differentiation 4 and 8 concentrations (CD4, CD8), and complete blood count were analyzed. Dexamethasone significantly (<i>p</i> &lt; 0.05) increased immobility time in behavioral tests, depleted serotonin and dopamine, elevated oxidative stress markers, and induced leukopenia with disrupted CD4/CD8 ratios. Lycopene co-treatment reversed behavioral despair, restored neurotransmitter homeostasis, attenuated oxidative-inflammatory cascades, normalized immune cell populations, and improved metabolic parameters. Lycopene provides integrated multi-system protection against glucocorticoid-induced neurobehavioral and immunological dysfunction, positioning it as a potential promising nutritional adjunct for patients requiring chronic corticosteroid therapy.</p>

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Lycopene attenuates dexamethasone induced depression like behavior and immunological dysfunction via restoration of neuro-immune-metabolic homeostasis in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月19日

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  • Hend A. Essa

摘要

Chronic glucocorticoid therapy, while clinically indispensable, often induces debilitating neuropsychiatric side effects, including depression-like behaviors, alongside systemic immunosuppression and metabolic dysfunction. The convergence of central neurotoxicity and peripheral immune dysregulation presents a unique therapeutic challenge requiring multi-target interventions. This study investigated the prophylactic efficacy of lycopene against dexamethasone-induced behavioral, neurochemical, oxidative, inflammatory, and immunological perturbations in rats. Thirty-two adult male Sprague-Dawley rats were randomly assigned to four groups (n = 8): normal control, dexamethasone (2 mg/kg/day/intraperitoneal), lycopene (10 mg/kg/day/orally), and dexamethasone+lycopene combination. Treatments were administered daily for 21 days. Behavioral assessments (forced swim test, tail suspension test) were conducted. In frontal cortex and hippocampal tissues, neurochemical markers (brain-derived neurotrophic factor, gamma-aminobutyric acid, and acetylcholinesterase activity), neurotransmitters (serotonin, dopamine), oxidative stress markers (malondialdehyde, nitric oxide, reduced glutathione, superoxide dismutase, catalase), inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6), and caspase-3 were quantified. In serum, fasting blood glucose, insulin, liver and kidney function markers, oxidative stress markers, inflammatory cytokines (interleukin-4, tumor necrosis factor-alpha, interferon-gamma), cluster of differentiation 4 and 8 concentrations (CD4, CD8), and complete blood count were analyzed. Dexamethasone significantly (p < 0.05) increased immobility time in behavioral tests, depleted serotonin and dopamine, elevated oxidative stress markers, and induced leukopenia with disrupted CD4/CD8 ratios. Lycopene co-treatment reversed behavioral despair, restored neurotransmitter homeostasis, attenuated oxidative-inflammatory cascades, normalized immune cell populations, and improved metabolic parameters. Lycopene provides integrated multi-system protection against glucocorticoid-induced neurobehavioral and immunological dysfunction, positioning it as a potential promising nutritional adjunct for patients requiring chronic corticosteroid therapy.