Capsicum Protects Against Rotenone-Induced Toxicity in Mice Brain Via Reduced Oxidative Stress and 5-Lipoxygenase Activation

Author(s): Omar M.E. Abdel-Salam, Amany A Sleem, Eman R. Youness, Noha N. Yassen, Nermeen Shaffie, Sayed A. El-Toumy

Objective: Is to investigate the effect of Capsicum annuum L extract for its ability to prevent neuronal degeneration in rotenone intoxicated mice.

Methods: Rotenone 1.5 mg/kg was subcutaneously given three times per week for two consecutive weeks. Starting from the first day of rotenone treatment, mice also received intraperitoneal injections of Capsicum extract (56 or 224 mg/kg). The brain and liver content of the lipid peroxidation product malondialdehyde (MDA), nitric oxide, reduced glutathione (GSH), paraoxonase 1 activity as well as brain cholinesterase and 5-lipoxygenase activities were determined. Histopathology and glial fibrillary acidic protein (GFAP) immunostaining in brain were also performed.

Results: Rotenone treatment caused significantly raised brain and liver MDA by 64.4% and 93.3% and nitric oxide by 77.8% and 40.3%, respectively. Reduced glutathione decreased by 45.4% and 24.3% and PON1 activity fell by 39.4% and 28.7% in both the brain and liver, respectively. Cholinesterase activity in brain was inhibited by 60.6% while 5-lipoxygenase increased by 38.9%. In brain tissue, Capsicum prevented the increase in MDA and nitric oxide levels. Capsicum also restored GSH, PON-1 activity and alleviated the increase in 5-lipoxygenase activity. Cholinesterase activity was almost restored to control value by the higher dose of Capsicum. In the liver tissue, Capsicum caused a significant decrease in MDA, and nitric oxide levels, and increased GSH. It also increased PON-1 activity. The neurotoxicity of rotenone was prevented by the administration of Capsicum extract which prevented the neuronal degeneration and restored GFAP positive cells.

Conclusions: Capsicum exerts a neuroprotective effect in rotenone intoxicated mice and this is likely to involve reduced oxidative stress and 5-lipoxygenase activation.

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