Tylvalosin exhibits anti-inflammatory property and attenuates acute lung injury in different models possibly through suppression of NF-κB activation

Zhao, Zhongchao; Tang, Xiangfang; Zhao, Xinghui; Zhang, Min-Hong; Zhang, Weijian; Hou, Shaohua; Yuan, Weifeng; Zhang, Hongfu; Shi, Lijun; Jia, Hong Peng; Li, Lin; Lai, Zhi Yang; Gao, Junfeng; Zhang, Keyu; Fu, Ling; Chen, Wei

doi:10.1016/j.bcp.2014.04.015

Cited by 69 publications

(48 citation statements)

References 37 publications

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“…It is well known that NF-κB is an important regulator of inflammatory mediators during inflammation (Yu et al, 2013;Zhao et al, 2014). Recent studies showed that NF-κB plays a critical role in microglial activation by regulating of inflammatory mediators NO, PGE 2 , TNF-α, and IL-1β production (Dang et al, 2014;Velagapudi et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-κB pathway

Zhou

Wang

et al. 2015

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 99%

Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-κB pathway

Zhou

Wang

et al. 2015

European Journal of Pharmacology

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“…17,18 Recognition of LPS by TLR4 could induce NF-kB and MAPK activation. 19,20 The expression of inflammatory mediators is mainly modulated by NF-kB and MAPK signalling pathways. 21 Normally, NF-kB is present in its inactive cytoplasmic form bound to the repressor of NF-kB (IkBs).…”

Section: Discussionmentioning

confidence: 99%

Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-κB and MAPK signalling pathway

Cao¹,

Zheng

et al. 2015

Archives of Oral Biology

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“…NF-jB has been identified as the main target for the treatment of inflammatory diseases [21,22]. To investigate the anti-inflammatory mechanism of linalool, the effects of linalool on LPS-induced NF-jB activation were detected.…”

Section: Discussionmentioning

confidence: 99%

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

Zhou

et al. 2015

Neurochem Res

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Linalool, a natural compound of the essential oils, has been reported to have anti-inflammatory effects. This study aimed to investigate the anti-inflammatory effects and mechanism of linalool in LPS-stimulated BV2 microglia cells. BV2 microglia cells were stimulated with LPS in the presence or absence of linalool. The production of inflammatory mediators TNF-α, IL-1β, NO, and PGE2 as well as Nrf2, HO-1 expression were detected. Our results showed that linalool inhibited LPS-induced TNF-α, IL-1β, NO, and PGE2 production in a dose-dependent manner. Linalool also inhibited LPS-induced NF-κB activation. Treatment of linalool induced nuclear translocation of Nrf2 and expression of HO-1. In addition, our results showed that the anti-inflammatory effect of linalool was attenuated by transfection with Nrf2 siRNA. In conclusion, these results suggested that linalool inhibits LPS-induced inflammation in BV2 microglia cells by activating Nrf2/HO-1 signaling pathway.

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Tylvalosin exhibits anti-inflammatory property and attenuates acute lung injury in different models possibly through suppression of NF-κB activation

Cited by 69 publications

References 37 publications

Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-κB pathway

Pinocembrin inhibits lipopolysaccharide-induced inflammatory mediators production in BV2 microglial cells through suppression of PI3K/Akt/NF-κB pathway

Tormentic acid inhibits LPS-induced inflammatory response in human gingival fibroblasts via inhibition of TLR4-mediated NF-κB and MAPK signalling pathway

Linalool Inhibits LPS-Induced Inflammation in BV2 Microglia Cells by Activating Nrf2

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