Neuroprotective and Therapeutic Effect of Caffeine on the Rat Model of Parkinson's Disease Induced by Rotenone

ABSTRACT

The present study aimed to investigate the protective and therapeutic effects of caffeine on rotenone-induced rat model of Parkinson's disease (PD). Rats were divided into control, PD model induced by rotenone (1.5 mg/kg intraperitoneally (i.p.) for 45 days), protected group injected with caffeine (30 mg/kg, i.p.) and rotenone for 45 days (during the development of PD model), and treated group injected with caffeine (30 mg/kg, i.p.) for 45 days after induction of PD model. The data revealed a state of oxidative and nitrosative stress in the midbrain and the striatum of animal model of PD as indicated from the increased lipid peroxidation and nitric oxide levels and the decreased reduced glutathione level and activities of glutathione-S-transferase and superoxide dismutase. Rotenone induced a decrease in acetylcholinesterase and Na⁺/K⁺-ATPase activities and an increase in tumor necrosis factor-α level in the midbrain and the striatum. Protection and treatment with caffeine ameliorated the oxidative stress and the changes in acetylcholinesterase and Na⁺/K⁺-ATPase activities induced by rotenone in the midbrain and the striatum. This was associated with improvement in the histopathological changes induced in the two areas of PD model. Caffeine protection and treatment restored the depletion of midbrain and striatal dopamine induced by rotenone and prevented decline in motor activities (assessed by open field test) and muscular strength (assessed by traction and hanging tests) and improved norepinephrine level in the two areas. The present study showed that caffeine offered a significant neuroprotection and treatment against neurochemical, histopathological, and behavioral changes in a rotenone-induced rat model of PD.

KEYWORDS:

• caffeine
• dopamine
• locomotor activity
• neuroinflammation
• oxidative stress
• Parkinson's disease

Declaration of interest

The authorsdeclarenoconflicts of interest.The authors alone are responsible for the content andwriting of the article.

Additional information

Notes on contributors

Yasser A. Khadrawy

Yasser A. Khadrawy, PhD, is a professor of neurophysiology in the Medical Physiology Department of National Research Centre, Egypt. He is interested in the fields of neurophysiology, neurodegenerative diseases using animal models, and neurotoxicology and laser applications in the field of neurodegenerative disorders. He has published more than 40 articles in reputable journals and has participated in many scientific projects.

Ahmed M. Salem

Ahmed M. Salem, PhD, is a professor of biochemistry in the Biochemistry Department of Ain Shams University, Cairo, Egypt.

Karima A. El-Shamy

Karima A. El-Shamy, PhD, is a professor of physiology in the Medical Physiology Department, Medical Division of National Research Centre, Giza, Egypt.

Emad K. Ahmed

Emad K. Ahmed, PhD, is a lecturer of biochemistry in the Biochemistry Department of Ain Shams University, Cairo, Egypt.

Nevein N. Fadl

Nevein N. Fadl, PhD, is an associate professor of physiology in the Medical Physiology Department, Medical Division of National Research Centre, Giza, Egypt.

Eman N. Hosny

Eman N. Hosny, PhD, is a lecturer of physiology in the Medical Physiology Department, Medical Division of National Research Centre, Giza, Egypt.