BML-111 inhibit H₂O₂-induced pyroptosis and osteogenic dysfunction of human periodontal ligament fibroblasts by activating the Nrf2/HO-1 pathway.

ABSTRACT:

Background

Periodontitis is a common and harmful chronic inflammatory oral disease, characterized by the destruction of periodontal soft and hard tissues. The NLRP3 inflammasome-related pyroptosis and human periodontal ligament fibroblasts (hPDLFs) osteogenic dysfunction are involved in its pathogenesis. Studies have shown that lipoxin A4 is an endogenous anti-inflammatory mediator and BML-111 is a lipoxin A4 analog, which was found to have potent and durable anti-inflammatory effects in inflammatory diseases, but the mechanism remains unclear. The purpose of this study was to investigate whether BML-111 inhibits H₂O₂-induced dysfunction of hPDLFs, attenuates inflammatory responses, and identifies the underlying mechanisms.

Methods

The oxidative stress

SUBMITTER: Xu Y 

PROVIDER: S-EPMC10773113 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature