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

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)
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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
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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
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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.