Flufenamic acid inhibits pyroptosis in ischemic flaps via the AMPK-TRPML1-Calcineurin signaling pathway.

ABSTRACT:

Background

Ischemic injury is a primary cause of distal flap necrosis. Previous studies have shown that Flufenamic acid (FFA) can reduce inflammation, decrease oxidative stress (OS), and promote angiogenesis, suggesting its potential role in protecting flaps from ischemic damage. This study investigated the effects and mechanisms of FFA in enhancing the survival of ischemic flaps.

Methods

The viability of ischemic flaps was evaluated using laser doppler blood flow (LDBF) and survival rates. We examined levels of pyroptosis, OS, transcription factor E3 (TFE3)-induced autophagy, and elements of the AMPK-TRPML1-Calcineurin pathway through western blotting (WB), immunofluorescence, molecular docking, cellular thermal shift assay (CETSA) and surface plasmon resonance.

Results<

SUBMITTER: Chen L 

PROVIDER: S-EPMC12253954 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature