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Immunohistochemical Studies on HDAC-4 in Experimentally Induced Parkinson's Diseases
Current Issue
Volume 3, 2015
Issue 3 (June)
Pages: 65-74   |   Vol. 3, No. 3, June 2015   |   Follow on         
Paper in PDF Downloads: 12   Since Aug. 28, 2015 Views: 1065   Since Aug. 28, 2015
Authors
[1]
Mohamed A. Akela, Zoology Department, Faculty of Science, Tanta University, Tanta, Egypt.
[2]
Saber A. Sakr, Zoology Department, Faculty of Science, Menofia University, Shbin Alkom, Egypt.
[3]
Wafaa M. Ebrahim, Biochemistry Department, Faculty of Medicine, Tanta University, Tanta, Egypt.
[4]
Ahmed A. Massoud, Zoology Department, Faculty of Science, Tanta University, Tanta, Egypt.
[5]
Ehab M. Tousson, Zoology Department, Faculty of Science, Tanta University, Tanta, Egypt.
[6]
Abdulaziz A. Akila, Bachelor of Medicine & Surgery, Batterjee Medical College, Jeddah, KSA.
Abstract
The environmental toxin hypothesis was dominant for much of the 20th century, and posits that PD-related neurodegeneration results from exposure to a dopaminergic neurotoxin. Living in a rural environment appears to confer an increased risk of PD, perhaps due to increased exposureto pesticide use and wood preservatives. Cigarette smoking and coffee drinking are inversely associated with the risk for the development of PD. 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 effect of butyric acid in PD experimental model through HDAC activities. The study was carried out on five rat groups, control group, Parkinsonism group, and sodium butyrate group, two Parkinson’s disease groups co-administered and post treated with sodium butyrate. Parkinsonism was induced by ip injection of paraquat. Laboratory measurements included serum HDAC activity and HDAC-4 antibody stain. PD group, PD co-administered and post treated with sodium butyrate showed significant increase in HDAC activity. Histological and Immunohistochemical investigate. The increments in HDAC activities are one 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. Further investigation is required by determining activity of HDAC to clarify its role in Parkinsonism.
Keywords
Parkinson’s Disease, Intra Peritoneal, Histone Deacetylase, Methy Phenyl Tetrahydro Pyridine, Histone Acetyl Transferase, Sodium Butyrate
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