Aging is a condition characterized by progressive decline in tissue homeostasis due, at least in part, to the accumulation of replicative, oxidative, and genotoxic stress over time. The activity of the transcription factor NF-κB is upregulated in both naturally aged mice and multiple progeroid mouse models of accelerated aging. Suppressing NF-κB activity genetically or pharmacologically has been shown to delay the onset and progression of aging pathology and therefore prolong the healthspan in progeroid mouse models. Here, we describe the methods for measuring aging endpoints along with NF-κΒ activation in mice, as well as after pharmacologic intervention to prevent NF-κB activation using a NEMO-binding domain (NBD)–protein transduction domain (PTD) fusion peptide.
|Original language||English (US)|
|Number of pages||15|
|Journal||Methods in Molecular Biology|
|State||Published - 2015|
Bibliographical notePublisher Copyright:
© Springer Science+Business Media New York 2015.
- Aging endpoints
- Mouse model of aging
- Stress response