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<p>Following traumatic brain injury (TBI), the progression of brain tissue injuries and subsequent psychiatric complications considerably affect the quality of life in humans. <i>Diosmin</i> (DM) is a flavonoid and has been demonstrated to improve cognitive deficit and amplify brain electrical activity in the rat model of traumatic brain injury.&#xa0;We aimed to explore the potential protective effects of DM on single-unit neuronal firing, as well as on motor function and behaviors related to depression and anxiety associated with TBI.&#xa0;Forty-eight Wistar rats were randomly divided into sham-operated, TBI, and TBI + DM (100&#xa0;mg/kg/day; P.O.) Groups. Depression and anxiety-like behaviors and motor function were evaluated through standard behavioral tests and Rotarod apparatus at scheduled points in time. We also measured the neuronal firing rate in the striatum.&#xa0;The results indicated that DM pretreatment significantly improved TBI-induced depression and anxiety-like behaviors (<i>P</i> &lt; 0.01), and motor coordination (<i>P</i> &lt; 0.05). The striatum neuronal firing rate in the TBI + DM Group was significantly higher than the TBI group (216 Vs 49.38&#xa0;Hz, <i>P</i> &lt; 0.001).&#xa0;The findings suggest that pretreatment with DM may offer protective benefits against TBI-associated behavioral deficits.</p>

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Behavioral deficits after traumatic brain injury: Neuroprotective effect of Diosmin

  • 期刊论文

  • 发表日期：

    2025年4月22日

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  • Vida Naderi boldaji,
  • Mohammad Ali Mirshekar,
  • Saiedeh Arabmoazzen,
  • Farzaneh Faraji Shahrivar

摘要

Following traumatic brain injury (TBI), the progression of brain tissue injuries and subsequent psychiatric complications considerably affect the quality of life in humans. Diosmin (DM) is a flavonoid and has been demonstrated to improve cognitive deficit and amplify brain electrical activity in the rat model of traumatic brain injury. We aimed to explore the potential protective effects of DM on single-unit neuronal firing, as well as on motor function and behaviors related to depression and anxiety associated with TBI. Forty-eight Wistar rats were randomly divided into sham-operated, TBI, and TBI + DM (100 mg/kg/day; P.O.) Groups. Depression and anxiety-like behaviors and motor function were evaluated through standard behavioral tests and Rotarod apparatus at scheduled points in time. We also measured the neuronal firing rate in the striatum. The results indicated that DM pretreatment significantly improved TBI-induced depression and anxiety-like behaviors (P < 0.01), and motor coordination (P < 0.05). The striatum neuronal firing rate in the TBI + DM Group was significantly higher than the TBI group (216 Vs 49.38 Hz, P < 0.001). The findings suggest that pretreatment with DM may offer protective benefits against TBI-associated behavioral deficits.