Journal
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
Volume 43, Issue 4, Pages 399-407Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10863-011-9362-7
Keywords
Genistein; Beta-amyloid peptide 25-35; Mitochondria; PC12 cells
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Funding
- National Natural Science Foundation of China [30972470, 30771802]
- National High Technology Research and Development Program of China [2010AA023003]
- Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality [PHR 201006112]
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The antioxidative properties of genistein (Gen) have been demonstrated by our previous studies and others, but its potential mechanism was not very clear. Because of the key role of mitochondria in oxidant production, we wondered if mitochondria were one of Gen's neuroprotective targets. In the present study we investigated whether Gen has protective effects on mitochondria damaged by A beta 25-35. PC12 cells were pre-incubated with or without Gen for 2 h followed by the incubation with 20 mu M A beta 25-35 for another 24 h before mitochondrial membrane fluidity (MMF), mitochondrial membrane potential (MMP), and mitochondrial redox state were measured. The results showed that Gen alleviated the decrease of MMF induced by A beta 25-35, and maintained the MMP. Additionally, Gen promoted the mitochondrial antioxidative capability through increasing the GSH/GSSG ratio, GPx activity and MnSOD protein expression in mitochondria. Moreover, Gen reversed the changes of ChAT mRNA and AChE mRNA expression in cells induced by A beta 25-35. These results suggested that Gen can protect the mitochondrial membrane and maintain redox state in mitochondria damaged by A beta 25-35.
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