In mouse N2a cells incubated with amyloid-beta, treatment with MitoQ, SS31 and resveratrol prevented the abnormal expression of peroxiredoxins and mitochondrial structural genes.
In plain wordsIn cells, treatment with SS31 and two other agents prevented amyloid-beta from disturbing the activity of protective and mitochondrial genes.
- Peptide
- Elamipretide (SS-31)
- Outcome
- IncreasePeroxiredoxin and mitochondrial structural gene expression
- Study
mousen: not reported in source
Mouse neuroblastoma (N2a) cells incubated with amyloid-beta- Comparator
- Amyloid-beta alone
- Outcome group
- Mitochondrial function · Nervous system and cognition
- Studied dose
- Dose not stated
Source sentences
abnormal expression of peroxiredoxins and mitochondrial structural genes were prevented
1 context sentence(design, population, supporting numbers)
Using electron and confocal microscopy, gene expression analysis, and biochemical methods, we studied mitochondrial structure and function and neurite outgrowth in N2a cells treated with MitoQ, SS31, and resveratrol, and then incubated with Abeta.