Journal
MOLECULAR NEUROBIOLOGY
Volume 53, Issue 10, Pages 6968-6981Publisher
HUMANA PRESS INC
DOI: 10.1007/s12035-015-9603-6
Keywords
NSAIDs; Ibuprofen; Proteasome; Mitochondrial dysfunction; Neurodegeneration; Ageing; Apoptosis
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Funding
- Department of Biotechnology, Government of India
- Ramalinganswami Fellowship from the Department of Biotechnology, Government of India [BT/RLF/Reentry/11/2010]
- Innovative Young Biotechnologist Award (IYBA) scheme from the Department of Biotechnology, Government of India [BT/06/IYBA/2012]
- University Grants Commission, Council of Scientific and Industrial Research, Government of India
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In routine course of life, nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed antipyretic, analgesic, and anti-inflammatory drugs. It is a well-proposed notion that treatment of NSAIDs may induce anti-proliferative effects in numerous cancer cells. Ibuprofen from isobutylphenylpropanoic acid is NSAID and used to relieve fever, pain, and inflammation. It is also used for juvenile idiopathic arthritis, rheumatoid arthritis, patent ductus arteriosus, and for pericarditis. Despite few emerging studies have expanded the fundamental concept that the treatment of NSAIDs influences apoptosis in cancer cells, however the NSAID-mediated precise mechanisms that determine apoptosis induction without producing adverse consequences in variety of cancer cells are largely unknown. In our present study, we have observed that ibuprofen reduces proteasome activity, enhances the aggregation of ubiquitylated abnormal proteins, and also elevates the accumulation of crucial proteasome substrates. Ibuprofen treatment causes mitochondrial abnormalities and releases cytochrome c into cytosol. Perhaps, the more detailed study is needed in the future to elucidate the molecular mechanisms of NSAIDs that can induce apoptosis without adverse effects and produce effective anti-tumor effects and consequently help in neurodegeneration and ageing.
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