Oxidative stress and DNA damage signalling in skeletal muscle in pressure-induced deep tissue injury.

The molecular mechanisms that contribute to the pathogenesis of pressure-induced deep tissue injury are largely unknown. This study tested the hypothesis that oxidative stress and DNA damage signalling mechanism in skeletal muscle are involved in deep tissue injury. Adult Sprague Dawley rats were subject to an experimental protocol to induce deep tissue injury.

Habitual exercise increases resistance of lymphocytes to oxidant-induced DNA damage by upregulating expression of antioxidant and DNA repairing enzymes.

The underlying mechanisms of adaptation from staying physically active are not completely revealed. This study examined the effects of 8 and 20 weeks of habitual voluntary exercise on the susceptibility of lymphocytes to oxidant-induced DNA damage, antioxidant enzyme activities in cardiac and skeletal muscles, and circulatory antioxidant profile. Forty young adult rats were randomly assigned to sedentary control and exercise groups for an experimental period of 8 or 20 weeks.

Protective effect of caspase inhibition on compression-induced muscle damage.

There are currently no effective therapies for treating pressure-induced deep tissue injury. This study tested the efficacy of pharmacological inhibition of caspase in preventing muscle damage following sustained moderate compression. Adult Sprague-Dawley rats were subjected to prolonged moderate compression.

Proteasome inhibition alleviates prolonged moderate compression-induced muscle pathology.

Background: The molecular mechanism initiating deep pressure ulcer remains to be elucidated. The present study tested the hypothesis that the ubiquitin proteasome system is involved in the signalling mechanism in pressure-induced deep tissue injury.

Methods: Adult Sprague Dawley rats were subjected to an experimental compression model to induce deep tissue injury.

Muscle apoptosis is induced in pressure-induced deep tissue injury.

Pressure ulcer is a complex and significant health problem. Although the factors including pressure, shear, and ischemia have been identified in the etiology of pressure ulcer, the cellular and molecular mechanisms that contribute to the development of pressure ulcer are unclear. This study tested the hypothesis that the early-onset molecular regulation of pressure ulcer involves apoptosis in muscle tissue.