International Journal of Clinical and Experimental Neurology
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International Journal of Clinical and Experimental Neurology. 2015, 3(1), 11-20
DOI: 10.12691/ijcen-3-1-3
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Epigenetic Study of Parkinson’s Disease in Experimental Animal Model

Afrah F Salama1, Wafaa Ibrahim2, Ehab Tousson3, , Saber Sakr4, Ahmed Masoud3, Mohamed A Akela3 and Mahmoud A. Abd El-Rahman1

1Biochemistry Section, Department of Chemistry

2Department of medical Biochemistry, Faculty of Medicine, Tanta University

3Department of Zoology, Faculty of Science

4Department of Zoology, Faculty of Science, Minoufiya University, Egypt

Pub. Date: February 12, 2015

Cite this paper:
Afrah F Salama, Wafaa Ibrahim, Ehab Tousson, Saber Sakr, Ahmed Masoud, Mohamed A Akela and Mahmoud A. Abd El-Rahman. Epigenetic Study of Parkinson’s Disease in Experimental Animal Model. International Journal of Clinical and Experimental Neurology. 2015; 3(1):11-20. doi: 10.12691/ijcen-3-1-3


Epigenetic modifications are defined as mechanisms that are able to modify the expression levels of selected genes without necessarily altering their DNA sequence, as histone tail modifications. These modifications are likely to contribute to the onset and progression of complex human diseases including neurodegenerative ones. Oxidative stress also is thought to be a common underlying mechanism that leads to cellular dysfunction and demise in PD. This study was aimed to assess the epigenetic fingerprint in PD experimental model through HDAC, PARP and activities oxidative stress markers. Materials and methods: The study was carried out on five rat groups, control group, Parkinsonism group, sodium butyrate group, two parkinson’s disease groups co-treated and post treated with sodium butyrate. Parkinsonism was induced by ip injection of paraquat. Laboratory measurements included serum 8-OHdG, MDA level as biomarkers of oxidative stress. HDAC and PARP activities were measured as other epigenetic mechanisms. Results: PD group, PD co-treated and post treated with sodium butyrate showed significant increase in HDAC and PARP activities. Also, there was significant increase in serum 8-OHdG level and MDA level in both serum and tissue. Conclusion and recommendations: The increments in HDAC and PARP activities are either two of the pathogenic mechanisms of the disease or it affords PD patients neuroprotection and benefits. Also, sodium butyrate is one of best antioxidant and neuroprotective agents. We recommended for further studies in HDAC and sodium butyrate as inhibitor in neurodegerative diseases, other diseases and normal state.

Parkinson’s disease Oxidative stress HDAC 8-OHdG Sodium butyrate

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