Animal models and experimental medicine · 2026
Multipathway modulation of neuroinflammation and oxidative stress by hesperidin in a rat single prolonged stress model of post-traumatic stress disorder.
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Anyanwu Godson Emeka, Akanaku Ogan Christopher, Oviosun Augustine, Ekwueme Precious E, Odey Paul Anyiom, Okechukwu Ugwu Chima Paul, Anyanwu Chinyere Nkemjika
Аннотация
BACKGROUND: Post-traumatic stress disorder (PTSD) is a complicated neuropsychiatric disorder that is marked by long-term neuroinflammation, oxidative stress, and poor neuroplasticity in stress-sensitive brain areas. Hesperidin is a citrus-derived flavanone glycoside that has been reported to have multitarget neuroprotective effects with antioxidant, anti-inflammatory, and neurotrophic regulatory activities. However, its integrated effects across convergent pathological pathways in validated PTSD models remain insufficiently defined.
METHODS: Male Wistar rats were subjected to the single prolonged stress (SPS) paradigm and treated with hesperidin (50, 100, and 200 mg/kg), fluoxetine (20 mg/kg), or vehicle for 14 days. Biochemical assessments (malondialdehyde [MDA], catalase [CAT], superoxide dismutase [SOD]) and immunohistochemical measurements of neuronal and glial integrity (NeuN, glial fibrillary acidic protein [GFAP], brain-derived neurotrophic factor [BDNF]) in the hippocampus, amygdala, and prefrontal cortex were performed.
RESULTS: SPS exposure induced marked oxidative imbalance, evidenced by increased MDA levels and reduced CAT activity, alongside significant upregulation of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-1β, increased astrocytic reactivity (GFAP), and reduced BDNF expression. Hesperidin treatment significantly attenuated lipid peroxidation, partially restored CAT activity, and suppressed pro-inflammatory cytokines, with the most pronounced effect observed for IL-1β. Notably, hesperidin reduced astrocytic activation and preserved neuronal morphology, while enhancing BDNF expression in a dose-dependent manner, with optimal effects at 50-100 mg/kg. Conversely, there was little group variation in the activity of SOD, implying pathway-selective redox regulation.
CONCLUSION: Hesperidin has multipathway, coordinated, modulatory effects on oxidative stress, neuroinflammation, glial activation, and neurotrophic signaling in the SPS model of PTSD. These findings support its utility as a mechanistic probe for interrogating convergent stress-related neuropathological pathways.
METHODS: Male Wistar rats were subjected to the single prolonged stress (SPS) paradigm and treated with hesperidin (50, 100, and 200 mg/kg), fluoxetine (20 mg/kg), or vehicle for 14 days. Biochemical assessments (malondialdehyde [MDA], catalase [CAT], superoxide dismutase [SOD]) and immunohistochemical measurements of neuronal and glial integrity (NeuN, glial fibrillary acidic protein [GFAP], brain-derived neurotrophic factor [BDNF]) in the hippocampus, amygdala, and prefrontal cortex were performed.
RESULTS: SPS exposure induced marked oxidative imbalance, evidenced by increased MDA levels and reduced CAT activity, alongside significant upregulation of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-1β, increased astrocytic reactivity (GFAP), and reduced BDNF expression. Hesperidin treatment significantly attenuated lipid peroxidation, partially restored CAT activity, and suppressed pro-inflammatory cytokines, with the most pronounced effect observed for IL-1β. Notably, hesperidin reduced astrocytic activation and preserved neuronal morphology, while enhancing BDNF expression in a dose-dependent manner, with optimal effects at 50-100 mg/kg. Conversely, there was little group variation in the activity of SOD, implying pathway-selective redox regulation.
CONCLUSION: Hesperidin has multipathway, coordinated, modulatory effects on oxidative stress, neuroinflammation, glial activation, and neurotrophic signaling in the SPS model of PTSD. These findings support its utility as a mechanistic probe for interrogating convergent stress-related neuropathological pathways.