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Front Immunol: Maf1 improves the occurrence of sepsis-related encephalopathy by inhibiting the NF-kB/NLRP3 inflammasome signaling pathway

 Last Update: 2021-08-03
 Source: Internet
 Author: User

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NOD-, LRR- and pyridine domain-containing protein 3 (NLRP3) inflammasomes have been identified as important mediators of blood-brain barrier destruction in sepsis-related encephalopathy (SAE)
.
However, there is currently no information on key upstream regulators of SAE

Researchers used lipopolysaccharide (LPS) to establish an in vitro model of blood-brain barrier (BBB) destruction and an in vivo model of SAE
.
The destruction of BBB integrity was assessed by measuring the expression level of tight junction proteins

The results showed that Maf1 significantly inhibited LPS-induced brain inflammation and nerve apoptosis in vivo and in vitro
.
It is worth noting that Maf1 reduced the activation of NLRP3 inflammasome and the expression of pro-inflammatory cytokines induced by NF-κB/p65

In summary, the results of this study indicate that regulating Maf1 may be a treatment strategy for SAE and other inflammation-related neurodegenerative diseases

Original source:

Shenglong Chen, et al.

Maf1 Ameliorates Sepsis-Associated Encephalopathy by Suppressing the NF- k B / NLRP3 Inflammasome Signaling Pathway In this message

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