Suppr超能文献

多巴胺 D1 受体激动剂 A-68930 抑制 NLRP3 炎性小体激活并保护大鼠免受脊髓损伤诱导的急性肺损伤。

Dopamine D1 receptor agonist A-68930 inhibits NLRP3 inflammasome activation and protects rats from spinal cord injury-induced acute lung injury.

作者信息

Jiang W, Li M, He F, Bian Z, Liu J, He Q, Wang X, Sun T, Zhu L

机构信息

Department of Orthopedics, Nanjing Medical University, Affiliated Hangzhou Hospital (Hangzhou First People's Hospital), Hangzhou, China.

Department of Orthopaedics, General Hospital of Beijing Military Command, Beijing, China.

出版信息

Spinal Cord. 2016 Nov;54(11):951-956. doi: 10.1038/sc.2016.52. Epub 2016 Apr 12.

Abstract

STUDY DESIGN

Randomized experimental study.

OBJECTIVES

The study aimed to investigate the therapeutic efficacy and molecular mechanisms of A-68930 in a rat model of spinal cord injury (SCI)-induced acute lung injury (ALI).

SETTING

China.

METHODS

The influences of A-68930 on the pulmonary edema, histological changes, proinflammatory cytokines levels, myeloperoxidase (MPO) activity and NLRP3 inflammasome protein expression were estimated.

RESULTS

SCI significantly promoted NLRP3 inflammasome activation, increased proinflammatory cytokine productions and MPO activity, and induced pulmonary edema and tissue damage in the SCI group as compared with the control group. A-68930 administration significantly inhibited NLRP3 inflammasome activation and reduced inflammatory cytokines levels and MPO activity. Moreover, A-68930 administration attenuated pulmonary edema and histopathology.

CONCLUSION

Our experimental findings indicated that A-68930 exhibited a protective effect on SCI-induced ALI by the alleviations of inflammatory response with the inhibition NLRP3 inflammasome activation 72 h post injury. The present study indicated that A-68930 could be a potentially efficient therapeutic strategy for the treatment of SCI-induced ALI.

摘要

研究设计

随机实验研究。

目的

本研究旨在探讨A - 68930对脊髓损伤(SCI)诱导的急性肺损伤(ALI)大鼠模型的治疗效果及分子机制。

研究地点

中国。

方法

评估A - 68930对肺水肿、组织学变化、促炎细胞因子水平、髓过氧化物酶(MPO)活性和NLRP3炎性小体蛋白表达的影响。

结果

与对照组相比,SCI显著促进了NLRP3炎性小体激活,增加了促炎细胞因子产生和MPO活性,并在SCI组诱导了肺水肿和组织损伤。给予A - 68930可显著抑制NLRP3炎性小体激活,降低炎性细胞因子水平和MPO活性。此外,给予A - 68930可减轻肺水肿和组织病理学变化。

结论

我们的实验结果表明,A - 68930通过在损伤后72小时抑制NLRP3炎性小体激活减轻炎症反应,对SCI诱导的ALI具有保护作用。本研究表明,A - 68930可能是治疗SCI诱导的ALI的一种潜在有效治疗策略。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验