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<p>Traumatic Brain Injury (TBI) is a debilitating neurological condition resulting from external mechanical forces, often leading to cognitive impairment, neuroinflammation, and oxidative stress. Current therapeutic strategies offer limited efficacy in reversing TBI-induced neuronal damage. Ashwagandha (<i>Withania somnifera</i>), a traditional Ayurvedic herb, is known for its neuroprotective and anti-inflammatory properties. This study aimed to evaluate the therapeutic potential of Ashwagandha in a controlled cortical impact (CCI)-induced TBI model in adult male C57BL/6 mice. Animals were divided into four groups: Sham Control, TBI Control, TBI + Vehicle, and TBI + Ashwagandha (500&#xa0;mg/kg body weight for 14 days post-injury). Behavioral assessments (Y-maze and Morris water maze) revealed that Ashwagandha significantly alleviated TBI-induced hyperactivity, though memory deficits persisted. Biochemical analyses showed a marked reduction in oxidative stress markers (Catalase, CAT, Superoxide dismutase SOD) and pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) in the Ashwagandha-treated group. Histopathological and immunohistochemical evaluations demonstrated preserved neuronal architecture and decreased astrocytic (GFAP) and microglial (Iba-1) activation. These findings indicate that Ashwagandha effectively mitigates neuroinflammation, reduces oxidative damage, and improves histological outcomes in TBI mice. In conclusion, Ashwagandha exhibits significant neuroprotective effects and may serve as a promising adjunct therapy for managing TBI-induced neuropathology.</p>

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Effects of Withania Somnifera on Stress Response, Neuroinflammation, and Brain Histopathology in a Mouse Model of Traumatic Brain Injury

  • 期刊论文

  • 发表日期：

    2026年5月28日

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  • Aishah E. Albalawi,
  • Fahad Eid Albalawi,
  • Ifat Alsharif,
  • Mashael A. Alotaibi,
  • Reem Hasaballah Alhasani,
  • Fatima S. Alaryani,
  • Zuhair M. Mohammedsaleh,
  • Tahani Ahmad ALMatrafi,
  • Suad Hamdan Almasoudi,
  • Amany I. Almars,
  • Areej M. Alshehri,
  • Fayez Alsulaimani,
  • Sawsan Abd Ellatif,
  • Mona H. Soliman,
  • Hailah M. Almohaimeed

摘要

Traumatic Brain Injury (TBI) is a debilitating neurological condition resulting from external mechanical forces, often leading to cognitive impairment, neuroinflammation, and oxidative stress. Current therapeutic strategies offer limited efficacy in reversing TBI-induced neuronal damage. Ashwagandha (Withania somnifera), a traditional Ayurvedic herb, is known for its neuroprotective and anti-inflammatory properties. This study aimed to evaluate the therapeutic potential of Ashwagandha in a controlled cortical impact (CCI)-induced TBI model in adult male C57BL/6 mice. Animals were divided into four groups: Sham Control, TBI Control, TBI + Vehicle, and TBI + Ashwagandha (500 mg/kg body weight for 14 days post-injury). Behavioral assessments (Y-maze and Morris water maze) revealed that Ashwagandha significantly alleviated TBI-induced hyperactivity, though memory deficits persisted. Biochemical analyses showed a marked reduction in oxidative stress markers (Catalase, CAT, Superoxide dismutase SOD) and pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) in the Ashwagandha-treated group. Histopathological and immunohistochemical evaluations demonstrated preserved neuronal architecture and decreased astrocytic (GFAP) and microglial (Iba-1) activation. These findings indicate that Ashwagandha effectively mitigates neuroinflammation, reduces oxidative damage, and improves histological outcomes in TBI mice. In conclusion, Ashwagandha exhibits significant neuroprotective effects and may serve as a promising adjunct therapy for managing TBI-induced neuropathology.