AI Article Synopsis
- The study investigated the potential of Puerarin to improve the survival of ischemic flaps, which are often limited in clinical use due to necrosis.
- Experimental procedures measured the effects of Puerarin on human umbilical vein endothelial cells and assessed flap viability using various techniques, revealing significant improvements in flap survivability.
- Results indicated that Puerarin enhances flap survival by promoting autophagy and reducing oxidative stress, with the AMPK-TRPML1-Calcineurin pathway playing a key role, suggesting its therapeutic potential for ischemic conditions.
Article Abstract
Background And Aim: Necrosis of random-pattern flaps restricts their application in clinical practice. Puerarin has come into focus due to its promising therapeutic effects in ischemic diseases. Here, we employed Puerarin and investigated its role and potential mechanisms in flap survival.
Experimental Procedure: The effect of Puerarin on the viability of human umbilical vein endothelial cells (HUVECs) was assessed by CCK-8, EdU staining, migration, and scratch assays. Survival area measurement and laser Doppler blood flow (LDBF) were utilized to assess the viability of ischemic injury flaps. Levels of molecules related to oxidative stress, pyroptosis, autophagy, transcription factor EB (TFEB), and the AMPK-TRPML1-Calcineurin signaling pathway were detected using western blotting, immunofluorescence, dihydroethidium (DHE) staining, RT-qPCR and Elisa.
Key Results: The findings demonstrated that Puerarin enhanced the survivability of ischemic flaps. Autophagy, oxidative stress, and pyroptosis were implicated in the ability of Puerarin in improving flap survival. Increased autophagic flux and augmented tolerance to oxidative stress contribute to Puerarin's suppression of pyroptosis. Additionally, Puerarin modulated the activity of TFEB through the AMPK-TRPML1-Calcineurin signaling pathway, thereby enhancing autophagic flux.
Conclusions And Implications: Puerarin promoted flap survival from ischemic injury through upregulation of TFEB-mediated autophagy and inhibition of oxidative stress. Our findings offered valuable support for the clinical application of Puerarin in the treatment of ischemic diseases, including random-pattern flaps.
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| http://dx.doi.org/10.1016/j.ejphar.2024.176621 | DOI Listing |
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