Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair.

ABSTRACT:

Background and purpose

NAD(+) is an essential cofactor for cellular energy production and participates in various signaling pathways that have an impact on cell survival. After cerebral ischemia, oxidative DNA lesions accumulate in neurons because of increased attacks by ROS and diminished DNA repair activity, leading to PARP-1 activation, NAD(+) depletion, and cell death. The objective of this study was to determine the neuroprotective effects of NAD(+) repletion against ischemic injury and the underlying mechanism.

Methods

In vitro ischemic injury was induced in rat primary neuronal cultures by oxygen-glucose deprivation (OGD) for 1 to 2 hours. NAD(+) was replenished by adding NAD(+) directly to the culture medium before or after OGD. Cell viability, oxidative DNA damage,

SUBMITTER: Wang S 

PROVIDER: S-EPMC2743302 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature