Abstract

Pressure ulcer is a complex and significant health problem in long-term bedridden patients, and there is currently no effective treatment or efficient prevention method. Furthermore, the molecular mechanisms and pathogenesis contributing to the deep injury of pressure ulcers are unclear. The aim of the study was to explore the role of endoplasmic reticulum (ER) stress and Akt/GSK3β signaling in pressure ulcers. A model of pressure-induced deep tissue injury in adult Sprague-Dawley rats was established. Rats were treated with 2-h compression and subsequent 0.5-h release for various cycles. After recovery, the tissue in the compressed regions was collected for further analysis. The compressed muscle tissues showed clear cellular degenerative features. First, the expression levels of ER stress proteins GRP78, CHOP, and caspase-12 were generally increased compared to those in the control. Phosphorylated Akt and phosphorylated GSK3β were upregulated in the beginning of muscle compression, and immediately significantly decreased at the initiation of ischemia-reperfusion injury in compressed muscles tissue. These data show that ER stress may be involved in the underlying mechanisms of cell degeneration after pressure ulcers and that the Akt/GSK3β signal pathway may play an important role in deep tissue injury induced by pressure and ischemia/reperfusion.

Highlights

  • A pressure ulcer is a localized tissue injury caused by the compression of underlying tissue with bony prominence pressure [1]

  • Tinhiutisa,lfrdoemsctrhipetoiountseotf, ipnrteascstusrekiunlcmerasylikneoltyardepeqreusaetnetlya dreefelepcttistshueeirintrjuurey,saenvderaitnyin[2it0i]a.lTdheescrerifpotrieo,nthoef ipnatathcot gskeinnesmisaoyfnmotuascdleeqtuisastueelys irneflDeTctI thhaesirretrcuenetslyevbeercitoym[e20a].foTchuesreinfoprere, sthsuerpeauthlcoegrerneesesiasrcohf.muscle tissueOsuinr DpTreIvhiaosursecreenstelayrbcheco[2m1e] ashfoocwusedin tphraetssauremuitlocecrhorensderairac-hm. ediated apoptotic pathway is activated in the development of early-stage PU after undergoing prolonged I/R procedures

  • Our previous research [21] showed that a mitochondria-mediated apoptotic pathway is activated in the development of early-stage PU after undergoing prolonged I/R procedures

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Summary

Introduction

A pressure ulcer is a localized tissue injury caused by the compression of underlying tissue with bony prominence pressure [1]. The National Pressure Ulcer Advisory Panel has improved the system for evaluating the stages of a pressure ulcer and described that deep tissue injury (DTI) is characterized by damage to the underlying soft tissue such as muscles. Subcutaneous soft tissue is an original site for pressure ulcers. This type of ulceration is severe and difficult to detect. When such an ulceration reaches an advanced stage, treatment becomes difficult and the prognosis is poor [2]. A superficial skin focus cannot represent the entirety of pressure-induced DTI [3,4]

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