Journal of Cellular & Molecular Anesthesia
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Evaluation of the Neuroprotective Effect of Chalcone on P53 and Caspase III Expression and D2-Like Dopaminergic Receptor Up-Regulation in vitro Parkinson's Model
Abstract
Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder of the central nervous system (CNS). Several studies indicated abnormal cell death in neurodegenerative diseases. Chalcone is a compound of natural origin with various properties such as antioxidant, anti-inflammatory, and inhibition of apoptosis. We investigated the impact of chalcone in an in-vitro model of PD.
Materials and Methods: PC12 cells were divided into four groups. Negative control, 6-hydroxy dopamine (6-OHDA) group (treatment with 75µM 6-OHDA), sham (treated with dimethyl sulfoxide), and the experimental groups with different dosages of chalcone treatment. Cell viability and reactive oxygen species (ROS) were assessed by MTT and ROS kit, respectively. The expressions of D2-like receptors, P53, and caspase III were evaluated by Western blotting.
Results: We found that 6-OHDA induced cytotoxicity and ROS production. The viability results showed that all doses of chalcone significantly increased viability after 48 hours compared to the control group (P<0.01). The western blotting results showed that caspase III and P53 expression decreased significantly in the experimental groups compared to the 6-OHDA group. However, D2-like receptor expression did not significantly differ between the experimental and the 6-OHDA group.
Conclusion: Complementary therapies, such as the use of antioxidants and the chalcone family, along with standard treatments for neurodegenerative diseases such as Parkinson's, may reduce the symptoms of the disease.
References
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Copyright
© 2023, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.
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