The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.

Abstract

Ischemic stroke, one of the world's leading fatal diseases, has a high incidence and recurrence, leading to severe mortality and disability. In this study, we investigated whether treadmill exercise is an important treatment to prevent recurrence and improve functional impairment following an ischemic stroke. Experimental cerebral ischemia by occluding the middle cerebral artery was induced in rats, and the effect of 10- or 30-min training for two weeks was evaluated. To assess for motor function improvement, behavioral tests including the elevated body swing test were conducted. The expressions of the endoplasmic reticulum (ER) stress and apoptosis markers were investigated by Western blotting analysis and immunohistochemistry. In both exercise groups (10 and 30 min), motor function improved compared to the non-exercise group. TTC staining demonstrated that the brain infarct volume also decreased after exercise. Further examination of the signaling pathway showed that the expression of ER stress-related proteins, such as IRE1-α, JNK, ERK, and p38 MAPK, decreased significantly in the exercise groups. The pro-apoptotic genes (Bax and pro-caspase3) of the apoptosis signaling mechanism, also decreased in the exercise groups. Interestingly, the level of neuronal markers (NeuN, SYP, and NFH) increased in the exercise groups. Our results suggest that exercise has a beneficial effect following ischemic stroke. In particular, exercise used in short- or long-term training could regulate the signaling mechanisms, such as ER stress, apoptosis, and neuronal cell death protection.