Neurotherapeutic Effects of Bee Venom in a Rotenone-Induced Mouse Model of Parkinson’s Disease

M. K. Rakha, The British University in Egypt
R. A. Tawfiq, The British University in Egypt
M. M. Sadek, The British University in Egypt
M. A. Anwer, The British University in Egypt
S. M. Salama, The British University in Egypt
A. F. Mohamed, The British University in Egypt
M. G. El-Hendy, The British University in Egypt
Sh E. El-Said, The British University in Egypt
N. M. Ahmed, The British University in Egypt
K. S. Mekawi, The British University in Egypt
A. M.Abd El-Aziz, The British University in Egypt
M. M. Elmazar, The British University in Egypt

Abstract

© 2019, Springer Science+Business Media, LLC, part of Springer Nature. Parkinson’s disease (PD) is a widespread progressive neurodegenerative disease; its main neuropathological hallmark is massive loss of dopaminergic neurons. Most PD studies were focused on the basal ganglia. However, the cerebral cortex, hippocampus, and striatum also play certain roles in PD pathophysiology. Dopamine replacement therapies remain the most effective clinical option for PD patients despite the occasional severe side effects. Bee Venom (BV) produced by Africanized honey bee, Apis mellifera L., is rich in neuroactive molecules; this venom is an irrefutable source of neuroprotectors and neuromodulators. In our study, we evaluated the neurotherapeutic effects of Egyptian BV against PD hallmarks in a PD mouse model. Six subcutaneous injections of 1.5 mg/kg of rotenone at 48-h-long intervals induced significant reductions in the motor strength and motor coordination. Additionally, significant declines in the dopamine level and total antioxidant capacity combined with significant elevation in interleukin 1β and interleukin 6 were observed. Rotenone-treated mice showed nuclear pyknosis and neuronal degeneration in the cerebral cortex and hippocampus, eosinophilic plaques, and hemorrhages in the striatum focal area and nuclear pyknosis and neuronal degeneration with diffuse gliosis in other brain structures. In rotenone-treated mice, i.p. injections of BV (6 doses 1.0 mg/kg at 24-h-long interval) recovered motor strength and motor coordination. Moreover, BV markedly increased the dopamine level and total antioxidant capacity. Also, BV greatly reduced the interleukin 1β and interleukin 6 contents. Furthermore, BV preserved neurons in the dentate gyrus of the hippocampus with no histopathological alterations. Besides, BV restricted nuclear pyknosis and neuronal degeneration in a few neurons in the cerebral cortex, hippocampus, and focal area of the striatum. Overall, BV may be a promising biotherapy for PD patients.