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Ghrelin alleviates traumatic brain injury-induced acute lung injury through pyroptosis/NF-κB pathway.

Ghrelin 通过焦亡/NF-κ b 通路减轻创伤性脑损伤诱导的急性肺损伤

  • 影响因子:3.32
  • DOI:10.1016/j.intimp.2019.106175
  • 作者列表:"Shao XF","Li B","Shen J","Wang QF","Chen SS","Jiang XC","Qiang D
  • 发表时间:2020-01-06
Abstract

:Acute lung injury (ALI) is one of the severe complications in patients with traumatic brain injury (TBI), contributing to the high mortality. Ghrelin has protective effects against various inflammatory diseases, but the effects of Ghrelin on TBI-induced ALI and its mechanisms remain unknown. In this study, Ghrelin administration was performed on the mice with TBI, then histological change in cortex and lung tissues, lung vascular permeability and macrophage number in bronchoalveolar lavage fluid (BALF) were examined, respectively. Simultaneously, the alterations of proinflammatory factors and pyroptosis-related proteins in lung tissues were detected. As a result, TBI-induced ALI was ameliorated after Ghrelin treatment, which was demonstrated by improved histology, reduced lung vascular permeability, and peripheral macrophage number. Furthermore, Ghrelin decreased the mRNA levels of proinflammatory factors (IL-1β, IL-6, TNF-α and IL-18), the protein levels of pyroptosis-related proteins (NLRP3, Caspase1-P20, HMGB1 and Gasdermin D), and the phosphorylation levels of NF-κB in lung tissues. These results showed that Ghrelin attenuating TBI-induced ALI might be via ameliorating inflammasome-induced pyroptosis by blocking NF-κB signal, which are important for the prevention and treatment of TBI-induced ALI.

摘要

急性肺损伤 (ALI) 是创伤性脑损伤 (TBI) 患者的严重并发症之一,病死率高。Ghrelin 对多种炎症性疾病具有保护作用,但 Ghrelin 对 TBI 诱导的 ALI 的影响及其机制尚不清楚。本研究对 TBI 小鼠进行 Ghrelin 治疗,检测皮层和肺组织的组织学变化,支气管肺泡灌洗液 (BALF) 中肺血管通透性和巨噬细胞数量。分别。同时检测肺组织中促炎因子和焦亡相关蛋白的变化。结果,Ghrelin 治疗后 TBI 诱导的 ALI 得到改善,表现为组织学改善、肺血管通透性降低和外周巨噬细胞数量减少。此外,Ghrelin 降低了促炎因子 (il-1 β 、 IL-6 、 TNF-α 和 IL-18) 的 mRNA 水平、焦亡相关蛋白 (NLRP3 、 Caspase1-P20 、 HMGB1 和 Gasdermin D),以及肺组织中 NF-κ b 的磷酸化水平。这些结果表明,Ghrelin 减轻 TBI 诱导的 ALI 可能是通过阻断 NF-κ b 信号来改善炎性体诱导的焦亡,这对于预防和治疗 TBI 诱导的 ALI 具有重要意义。

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DOI:10.1042/BST20191010
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