Rotenone-induced energy stress decompensated in ventral mesocerebrum is associated with Parkinsonism progression in rats

Bai,Qunhua; He,Junlin; Tang,Yong; Wang,Shibo; Qiu,Jingfu; Wang,Yang; Yu,Chao

doi:10.3892/etm.2016.3352

Rotenone-induced energy stress decompensated in ventral mesocerebrum is associated with Parkinsonism progression in rats

Authors:
- Qunhua Bai
- Junlin He
- Yong Tang
- Shibo Wang
- Jingfu Qiu
- Yang Wang
- Chao Yu
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Affiliations: School of Public Health and Management, Chongqing Medical University, Chongqing 400016, P.R. China, Department of Spinal Cord Injury, Chongqing Orthopedics Hospital of Traditional Chinese Medicine, Chongqing 400016, P.R. China, Department of Infection Management, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China, Institute of Life Science, Chongqing Medical University, Chongqing 400016, P.R. China
Published online on: May 18, 2016 https://doi.org/10.3892/etm.2016.3352
Pages: 1060-1066

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Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disorder, which is characterized by the hallmark feature of loss of dopaminergic neurons in the substantia nigra. Energy metabolic disorder is associated with the pathogenesis of PD; however, the development of this disorder is yet to be elucidated. PD‑like characteristics have been demonstrated in a rotenone rat model. In the present study, energy metabolism status was investigated in a rat model following intraperitoneal treatment with 1.0 mg/kg rotenone every 48 h. The behavior and tyrosine hydroxylase‑positive levels in the substantia nigra of rats that were treated with rotenone for 24 weeks demonstrated that these rats developed more severe parkinsonism, as compared with that were treated for 16 weeks. Detection of ATP, lactic acid, NADH dehydrogenase 1 mRNA and lactate dehydrogenase B mRNA levels in the ventral mesocerebrum (VM) and skeletal muscle (SM) of the rats that had been treated with rotenone for 16 and 24 weeks demonstrated that the energy stress induced by rotenone progressed in both VM and SM. Notably, the energy stress detected in VM was more severe, and this energy stress was decompensated in the VM of rats that had been treated with rotenone for 24 weeks. The progression of energy stress and the incidence of energy decompensation in VM may be important for the improvement of PD pathology.

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