AI Article Synopsis
- The study investigates how curcumin affects the formation of oligomers and mitochondrial KATP channels (mitoKATP) related to α-synuclein overexpression or mutation, which are factors in neurodegenerative diseases.
- Using PC12 cells, the research demonstrates that curcumin significantly reduces oligomer formation and apoptosis, as indicated by decreased lactate dehydrogenase activity and increased mitochondrial membrane potential.
- The findings suggest that curcumin could serve as a protective agent by stabilizing mitoKATP channels, potentially mitigating the cytotoxic effects caused by α-synuclein mutations or overexpression.
Article Abstract
Objective: To investigate the effect of curcumin on oligomer formation and mitochondrial ATP-sensitive potassium channels (mitoKATP) induced by overexpression or mutation of α-synuclein.
Methods: Recombinant plasmids α-synuclein-pEGFP-A53T and α-synuclein-pEGFP-WT were transfected into PC12 cells by lipofectamin method, and intervened by application of curcumin (20 μmol/L) and 5-hydroxydecanoate (5-HD). Oligomer formation in the cultured cells was identified by Western blotting and Dot blotting. Cytotoxicity and apoptosis of the PC12 cells were measured by lactate dehydrogenase (LDH) and JC-1 assays. mitoKATP were identified by Western blotting and whole cell patch clamp.
Results: Curcumin has significantly reduced the oligomer formation induced by overexpression or mutation of α-synuclein in the cultured cells. LDH has decreased by 36.3% and 23.5%, and red/green fluorescence ratio of JC-1 was increased respectively by 48.46% and 50.33% after application of curcumin (P<0.05). Protein expression of Kir6.2 has decreased and mitoKATP channel current has significantly increased (P<0.05).
Conclusion: Curcumin can inhibit α-synuclein gene overexpression or mutation induced α-synuclein oligomers formation. It may block apoptosis induced by wild-type overexpression or mutation of α-synuclein. By stabilizing mitochondrial membrane potential. Opening of mitoKATP channel may have been the initiating protective mechanism of apoptosis induced by wild-type overexpression or mutation of α-synuclein. Curcumin may antagonize above cytotoxicity through further opening the mitoKATP channel.
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| http://dx.doi.org/10.3760/cma.j.issn.1003-9406.2015.04.002 | DOI Listing |
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