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乔松素通过抑制 TLR4-NF-κB-NLRP3 炎症小体信号通路缓解脂多糖和博来霉素诱导的肺炎症。

Pinocembrin relieves lipopolysaccharide and bleomycin induced lung inflammation via inhibiting TLR4-NF-κB-NLRP3 inflammasome signaling pathway.

机构信息

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300353, China.

State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300353, China; Tianjin Key Laboratory of Molecular Drug Research, Tianjin International Joint Academy of Biomedicine, Tianjin 300457, China.

出版信息

Int Immunopharmacol. 2021 Jan;90:107230. doi: 10.1016/j.intimp.2020.107230. Epub 2020 Dec 9.

Abstract

Inflammation is a defense response of the body to stimuli. Lung injury caused by external stimuli can stimulate inflammatory cells to accumulate at the site of injury and secrete cytokines. Pinocembrin is a flavonoid with anti-inflammatory effects. Based on previous studies, we further explored the anti-inflammatory mechanisms of pinocembrin in vitro and in vivo. In vitro studies indicated that pinocembrin inhibited lipopolysaccharide (LPS)-stimulated inflammatory response in macrophages. In vivo studies also showed that pinocembrin could reduce LPS and bleomycin (BLM) induced lung inflammatory response in mice. Further mechanistic studies indicated that pinocembrin could regulate the TLR4-NF-κB signaling pathway and suppressed the activation and assembly of NLRP3 inflammasomes. In summary, pinocembrin could relieve pulmonary inflammatory response induced by LPS and BLM mainly via inhibiting TLR4-NF-κB-NLRP3 inflammasome axis. These results contribute to the understanding of the anti-inflammatory mechanisms of pinocembrin and serve as reference for future research on pinocembrin.

摘要

炎症是机体对外界刺激的防御反应。外界刺激引起的肺损伤可刺激炎症细胞在损伤部位聚集并分泌细胞因子。乔松素是一种具有抗炎作用的类黄酮。基于之前的研究,我们进一步探讨了乔松素在体外和体内的抗炎机制。体外研究表明,乔松素抑制脂多糖(LPS)刺激的巨噬细胞炎症反应。体内研究也表明,乔松素可以减轻 LPS 和博来霉素(BLM)诱导的小鼠肺部炎症反应。进一步的机制研究表明,乔松素可以调节 TLR4-NF-κB 信号通路,并抑制 NLRP3 炎性小体的激活和组装。总之,乔松素主要通过抑制 TLR4-NF-κB-NLRP3 炎性小体轴来缓解 LPS 和 BLM 诱导的肺部炎症反应。这些结果有助于理解乔松素的抗炎机制,并为乔松素的未来研究提供参考。

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