Research ReportAutophagy suppression by exercise pretreatment and p38 inhibition is neuroprotective in cerebral ischemia

- Exercise and p38 inhibition suppressed p62 degradation by autophagy after ischemia.
- Exercise and p38 inhibition up-regulated the activation of ERK1/2 after ischemia.
- Suppression of autophagy by EX & p38IN benefited outcome of cerebral ischemia.

Autophagy is a degradative mechanism for cellular proteins and organelles, but its role in the nervous system is still not clear. In the present study, we found that exercise pretreatment and p38 inhibition had influence on autophagic process after cerebral ischemia, contributing to their neuroprotective effects. We examined the levels of p62 and phosphorylated ERK1/2 as an autophagic marker and cell-survival marker respectively after cerebral ischemic injury. The brain infarction volume after ischemia was measured as well. Both treadmill training pretreatment and p38 inhibition decreased the degradation of p62, promoted the phosphorylation of ERK1/2, and alleviated the brain infarction, indicating that these treatments could provide neuroprotection in cerebral ischemic injury via autophagy suppression.