Protective effect of Nigella sativa phytochemical thymoquinone in a mouse model of brain injury induced by potassium dichromate

Document Type : Research Paper

Authors

1 School of Medicine, Shahed University, Tehran, Iran

2 Department of Anatomy, School of Medicine, Shahed University, Tehran, Iran.

3 Neurophysiology Research Center, Shahed University, Tehran, Iran

Abstract

Background and Objective: Potassium dichromate, which is a form of hexavalent chromium, has been demonstrated to induce toxicity associated with oxidative stress in humans and animals. Thymoquinone (TQ) isolated from Nigella sativa has a wide spectrum of activities such as antioxidant, anti-inflammatory and anticancer effects. This study aimed to evaluate the protective effect of thymoquinone in an animal model of brain damage caused by potassium dichromate in the mouse.
Materials and Methods: In this study, mice were divided into 5 groups: control, control treated with 5 mg/kg thymoquinone, potassium dichromate, and potassium dichromate treated with 1 or 5 mg/kg thymoquinone. To induce neuronal injury, 0.5 mg/kg potassium dichromate was intranasally and daily administrated for two months. Thymoquinone was given orally and daily for seven weeks. After two months, activity of catalase (CAT), level of malondialdehyde (MDA), glutathione (GSH) and nitrite (Nit), and number of neurons in the parietal cortex were evaluated. Data analysis was conducted using one-way ANOVA and Tukey post-test with p<0.05 as significant.
Results: Potassium dichromate significantly lowered activity of CAT and elevated levels of MDA and Nit, reduced GSH level and decreased neuronal density in the parietal cortex. Treatment with 5 mg/kg thymoquinone significantly increased activity of CAT and reduced MDA level, elevated level of GSH and also prevented reduction of neuronal density in the parietal cortex.
Conclusion: Thymoquinone administration can lower oxidative stress and brain injury following potassium dichromate.

Keywords

References

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Journal of Basic and Clinical Pathophysiology
Volume 12, Issue 2
October 2024
Pages 29-37

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