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Published:
Mar 24, 2026DOI:
10.4314/tjpr.v25i2.9Keywords:
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Main Article Content
Effectiveness of thymoquinone for inhibiting the inflammation process in brain damage: Study in Wistar rats with intracerebral hemorrhage model
Abstract
Purpose: To evaluate the effectiveness of thymoquinone (TQ) in inhibiting inflammation and promoting neuronal regeneration in a Wistar rat model of intracerebral hemorrhage (ICH).
Methods: Thirty-three male Wistar rats were randomly divided into three groups (n = 11 each): Group 1 was ICH control (0.16 mL autologous blood injected into the brain). Group 2 is ICH + TQ 150 mg/kg/day, while Group 3 was ICH + TQ 250 mg/kg/day. Thymoquinone was administered orally for 3 days post-ICH. On day 3, brains were harvested and analyzed using hematoxylin-eosin staining and immunohistochemistry for Tumor necrosis factor-alpha (TNF-α), Ki-67, Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) and neuronal markers.
Results: Thymoquinone treatment resulted in significant dose-dependent neuroprotective effects. Compared to ICH control group (TNF-α: 10.20 ± 0.85; NeuN-positive neurons: 4.20 ± 0.79), the 250 mg/kg dose of TQ significantly reduced TNF-α levels to 3.73 ± 0.58 and increased NeuN-positive cell counts to 11.36 ± 1.24 (p < 0.05). The increase in NeuN-positive cells reflects enhanced neuronal survival (neuroprotection) rather than proliferation of post-mitotic neurons. Furthermore, TQ administration significantly upregulated PPARγ (10.82 ± 1.05) and Ki-67 (10.64 ± 1.12) expression. The elevation of Ki-67 within this 3-day window primarily indicates early reparative proliferation of glial cells and neural progenitors.
Conclusion: Thymoquinone significantly inhibits post-ICH neuroinflammation (via reduced TNF-α) and enhances neuronal regeneration, via increased Ki-67, PPARγ, and neuron count, in a dose-dependent manner. The 250 mg/kg dose is more effective in supporting TQ as a promising neuroprotective agent in ICH.
