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<p>The dysregulation of monoaminergic and GABAergic systems is associated with post-traumatic stress disorder (PTSD), warranting exploration of novel therapeutic agents. This study investigated the neuroprotective effects of hesperidin, a citrus flavonoid in a single prolonged stress (SPS)–induced rat model of PTSD. Thirty male Wistar rats were randomly distributed to six groups as follows: control, SPS-only, SPS + fluoxetine (10&#xa0;mg/kg), and SPS + hesperidin at 50&#xa0;mg/kg, 100&#xa0;mg/kg, and 200&#xa0;mg/kg groups. SPS entailed restraint, forced swim, anesthesia-ether, and isolation 7&#xa0;days. The duration of administration of the treatment administered was 14&#xa0;days. Behavioral tests (Elevated Plus Maze, Open Field Test, Sucrose Preference Test, and Tail Suspension Test), were performed at specific intervals. Neurochemical analysis of brain tissue included serotonin (5-HT), norepinephrine (NE), dopamine (DA), and GABA, along with their biosynthetic enzymes: TPH, TH, DBH, and GAD. Exposure to SPS decreased the number of open-arm entries, locomotion and sucrose preference, and increased the number of immobile behaviors, depicting anxiogenic, anhedonic, depressive-like behavior. At the neurochemical level, SPS induced a decrease in 5-HT, NE and enzymes (TPH, TH, DBH) and an increase in GAD. Hesperidin in dose-dependent manner was found to counter behavioral and neurochemical impairments and results of 100 and 200&#xa0;mg/kg hesperidin had similar effects to fluoxetine (<i>p</i> &lt; 0.05). Pearson correlations showed that neurotransmitters and their enzymes of biosynthesis had good positive correlations (e.g., TPH-5-HT: <i>r</i> = 0.77, <i>p</i> &lt; 0.01), suggesting that hesperidin restores neurotransmitter balance partly by supporting enzyme activity. Conclusively, hesperidin has a high level of anxiolytic and antidepressant-like effects in the PTSD model, which is likely associated with monoamine production route and the modulation of GABAergic tone. The above evidence proves its promise as a neurotherapeutic drug on stress-linked diseases.</p>

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Hesperidin reverses behavioral deficits and neurochemical disruptions in a single prolonged stress-induced PTSD rat model: targeting monoaminergic and GABAergic systems

  • 期刊论文

  • 发表日期：

    2025年11月1日

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  • Godson Emeka Anyanwu,
  • Ogan Christopher Akanaku,
  • Vivian Onyinye Ojiakor,
  • Usman Michael Ibe,
  • Chinyere Nkemjika Anyanwu

摘要

The dysregulation of monoaminergic and GABAergic systems is associated with post-traumatic stress disorder (PTSD), warranting exploration of novel therapeutic agents. This study investigated the neuroprotective effects of hesperidin, a citrus flavonoid in a single prolonged stress (SPS)–induced rat model of PTSD. Thirty male Wistar rats were randomly distributed to six groups as follows: control, SPS-only, SPS + fluoxetine (10 mg/kg), and SPS + hesperidin at 50 mg/kg, 100 mg/kg, and 200 mg/kg groups. SPS entailed restraint, forced swim, anesthesia-ether, and isolation 7 days. The duration of administration of the treatment administered was 14 days. Behavioral tests (Elevated Plus Maze, Open Field Test, Sucrose Preference Test, and Tail Suspension Test), were performed at specific intervals. Neurochemical analysis of brain tissue included serotonin (5-HT), norepinephrine (NE), dopamine (DA), and GABA, along with their biosynthetic enzymes: TPH, TH, DBH, and GAD. Exposure to SPS decreased the number of open-arm entries, locomotion and sucrose preference, and increased the number of immobile behaviors, depicting anxiogenic, anhedonic, depressive-like behavior. At the neurochemical level, SPS induced a decrease in 5-HT, NE and enzymes (TPH, TH, DBH) and an increase in GAD. Hesperidin in dose-dependent manner was found to counter behavioral and neurochemical impairments and results of 100 and 200 mg/kg hesperidin had similar effects to fluoxetine (p < 0.05). Pearson correlations showed that neurotransmitters and their enzymes of biosynthesis had good positive correlations (e.g., TPH-5-HT: r = 0.77, p < 0.01), suggesting that hesperidin restores neurotransmitter balance partly by supporting enzyme activity. Conclusively, hesperidin has a high level of anxiolytic and antidepressant-like effects in the PTSD model, which is likely associated with monoamine production route and the modulation of GABAergic tone. The above evidence proves its promise as a neurotherapeutic drug on stress-linked diseases.