Inhibition of Endoplasmic Reticulum Stress Alleviates Lung Injury Induced by Brain Death

Inflammation. 2017 Oct;40(5):1664-1671. doi: 10.1007/s10753-017-0606-5.

Abstract

Brain death (BD) can induce inflammation and injury of organs. Endoplasmic reticulum (ER) stress is associated with a variety of diseases. However, little is known about how ER stress is implicated in brain death (BD)-induced lung injury. In this study, a stable BD rat model was constructed to investigate the role of ER stress on BD-induced lung injury. H&E staining demonstrated that BD can induce lung injury in rats. The results of Western blot and immunohistochemistry showed that apoptosis was observed in the lung tissues of BD rats. And the level of GRP78, p-PERK, p-eIF2α, CHOP, and Caspase-12 was highly expressed in BD rats compared with the control group. Inhibition of ER stress with salubrinal reduced the BD-induced lung inflammation. Moreover, BD-induced increase of NF-κB activity was lowered by inhibition of ER stress. These results suggested that inhibition of ER stress alleviates BD-induced lung inflammation by regulating NF-κB signaling pathway.

Keywords: brain death; endoplasmic reticulum stress; inflammation; lung injury.

MeSH terms

  • Animals
  • Apoptosis
  • Brain Death / pathology*
  • Cinnamates / pharmacology
  • Endoplasmic Reticulum Stress / drug effects*
  • Inflammation
  • Lung Injury / etiology*
  • Lung Injury / pathology
  • NF-kappa B / drug effects
  • Rats
  • Thiourea / analogs & derivatives
  • Thiourea / pharmacology

Substances

  • Cinnamates
  • NF-kappa B
  • salubrinal
  • Thiourea