2023
DOI: 10.1016/j.phymed.2022.154489
|View full text |Cite
|
Sign up to set email alerts
|

Schisandrin B protects against LPS-induced inflammatory lung injury by targeting MyD88

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
4
0

Year Published

2023
2023
2024
2024

Publication Types

Select...
8

Relationship

0
8

Authors

Journals

citations
Cited by 14 publications
(4 citation statements)
references
References 44 publications
0
4
0
Order By: Relevance
“…Foreign inflammation-inducing substances such as LPS can initiate the downstream NF-κB/MAPK inflammatory cascade by binding to the transmembrane protein TLR4 on the cell surface, which promotes gene transcription and protein expression of inflammation-related factors, resulting in the development of the body’s inflammatory response [ 39 ]. The time-course data indicated that FLs blocked the activation of TLR4 from 0.5 h ( Figure 4 ).…”
Section: Resultsmentioning
confidence: 99%
“…Foreign inflammation-inducing substances such as LPS can initiate the downstream NF-κB/MAPK inflammatory cascade by binding to the transmembrane protein TLR4 on the cell surface, which promotes gene transcription and protein expression of inflammation-related factors, resulting in the development of the body’s inflammatory response [ 39 ]. The time-course data indicated that FLs blocked the activation of TLR4 from 0.5 h ( Figure 4 ).…”
Section: Resultsmentioning
confidence: 99%
“…LPS is an important factor in triggering pneumonia and has been widely studied for its potential to cause endothelial barrier dysfunction; it can effectively activate immune cells via TLR-4 and induce a variety of pro-inflammatory mediators and cytokines through different signaling pathways [6,31]. The inflammation mediation is closely related to the TLR-4/MyD88/MAPK signaling pathway [32,33]. New anti-inflammatory drugs are being discovered based on the inhibition of the TLR-4/MyD88/MAPK signaling pathway.…”
Section: Discussionmentioning
confidence: 99%
“…Prior investigations have indicated that the induction of TLR4 leads to the modulation of pro-inflammatory cytokine expression, which is primarily achieved via MyD88-dependent or MyD88-independent signaling cascades [ 24 ]. TLR4 can interact with MyD88 to stimulate TAK1, resulting in the initiation of NF-κB and MAPK signaling cascades that regulate pro-inflammatory factor ( Tnf-α, Ccl4, Ccl3 ) expression [ 25 ]. Moreover, TLR4 binding to TRIF induces activation of TBK1, thereby prompting IRF3 activation and the subsequent production of pro-inflammatory cytokines ( Cxcl9, Cxcl10, Il-11 ) [ 26 ].…”
Section: Discussionmentioning
confidence: 99%