Exercise Preconditioning Protects against Spinal Cord Injury in Rats by Upregulating Neuronal and Astroglial Heat Shock Protein 72

Abstract

The heat shock protein 72 (HSP 72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercised rats (given pre-SCI exercise) had significantly higher levels of neuronal and astroglial HSP 72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non-exercised rats. pSUPER plasmid expressing HSP 72 small interfering RNA (SiRNA-HSP 72) was injected into the injured spinal cords. In addition to reducing neuronal and astroglial HSP 72, the (SiRNA-HSP 72) significantly attenuated the beneficial effects of exercise preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP 72 in the gray matter of normal spinal cord tissue, exercise preconditioning promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP 72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP 72 in protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP 72-mediated exercise preconditioning is a promising strategy for facilitating functional recovery from SCI.

D‐β‐hydroxybutyrate promotes functional recovery and relieves pain hypersensitivity in mice with spinal cord injury

“…It was reported that dietary restriction (Plunet et al, ), intermittent fasting (Jeong et al, ), ketogenic diet (Streijger et al, ) and exercise (Chang et al, ) improved functional recovery after contusion SCI. Interestingly, D‐β‐hydroxybutyrate (DBHB) levels were elevated during prolonged exercise, starvation or by the low carbohydrate ketogenic diet (Cotter et al, ).…”

Effects of voluntary exercise on apoptosis and cortisol after chronic restraint stress in mice

“…In this study, there was no difference in the expression levels of HSP70 among the three groups, although its level was increased by RS. HSP70 can suppress stress-induced myocardial apoptosis through interaction with FAF-1 35 and stress protein marker HSP 72, resulted in apoptosis suppression in exercised rats 9 . Our results suggest that chronic restraint stress can trigger stress, the lead cause of apoptosis.…”

“…Restraint stress is greater than the stress caused by forced swimming exercise 2 . Heat shock protein 72 (HSP 70), a representative marker of stress protein, can be increased by exercise 9 . Exercise can also increases the expression levels of superoxide dismutase of Mn isoform (Mn-SOD), Bax, and caspase-3 protein that inhibit apoptosis in aged rat heart 10 .…”

Exercise in multiple sclerosis and its models: Focus on the central nervous system outcomes

“…These results were replicated in a study using 6 weeks of voluntary wheel running in aged APP/PS1 mice, except decreased microgliosis was also observed (He et al, 2017). Three weeks of swimming training prior to SCI in Sprague-Dawley rats significantly increased astrocyte proliferation and expression of HSP72, a protein purported to aid in reducing neuronal and astrocytic apoptosis (Chang et al, 2014).…”