Department of Hepatobiliary and Pancreatic Surgery, the First Affiliated Hospital of Zhengzhou University, No.1, East Jian She Road, Zhengzhou, Henan Province, 450052, China.
Henan Key Laboratory of Digestive Organ Transplantation, No.1, East Jian She Road, Zhengzhou, Henan Province, 450052, China.
Inflammation. 2017 Oct;40(5):1664-1671. doi: 10.1007/s10753-017-0606-5.
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.
脑死亡（BD）可引起器官炎症和损伤。内质网（ER）应激与多种疾病有关。然而，关于 ER 应激如何参与脑死亡（BD）诱导的肺损伤知之甚少。在这项研究中，构建了稳定的 BD 大鼠模型，以研究 ER 应激在 BD 诱导的肺损伤中的作用。H&E 染色表明 BD 可诱导大鼠肺损伤。Western blot 和免疫组化结果表明，BD 大鼠的肺组织中观察到细胞凋亡。与对照组相比，GRP78、p-PERK、p-eIF2α、CHOP 和 Caspase-12 的水平在 BD 大鼠中高表达。用 salubrinal 抑制 ER 应激可减轻 BD 诱导的肺炎症。此外，抑制 ER 应激降低了 BD 诱导的 NF-κB 活性增加。这些结果表明，抑制 ER 应激通过调节 NF-κB 信号通路缓解 BD 诱导的肺炎症。
