2. Academic Validation
  3. Pharmacodynamic insights into maresin 1: Enhancing flap viability via the keap1/Nrf2 axis to control ROS-driven apoptosis and ferroptosis

Pharmacodynamic insights into maresin 1: Enhancing flap viability via the keap1/Nrf2 axis to control ROS-driven apoptosis and ferroptosis

  • Eur J Pharm Sci. 2024 Dec 1:203:106923. doi: 10.1016/j.ejps.2024.106923.
Pin Fang 1,  Sheng Cheng 1,  Yingying Lai 1,  Xianhui Ma 1,  Keyu Lu 1,  Jingzhou Lu 1,  Guangyao Li 1,  Enhui Yang 2,  Ningning Yang 1,  Weiyang Gao 3,  Renhao Jiang 4
Affiliations

Affiliations

  • 1 Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; Zhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, China.
  • 2 Institute of Albert, Wenzhou Medical University, Wenzhou, China.
  • 3 Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; Zhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, China. Electronic address: weiyanggaoi@126.com.
  • 4 Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; Zhejiang Provincial Key Laboratory of Orthopaedics, Wenzhou, China; The Second School of Medicine, Wenzhou Medical University, Wenzhou, China. Electronic address: jiangrenhaofey@163.com.
PMID: 39368783 DOI: 10.1016/j.ejps.2024.106923
Abstract

Random flaps are widely used in tissue reconstruction, but the high incidence of FLAP necrosis after operation remains a significant challenge. Maresin 1 (MaR1), a mediator derived from docosahexaenoic acid, has been shown to have significant effects in resolving inflammation and promoting tissue regeneration. This study investigated the role of MaR1 in the survival of random flaps. Histological analysis, laser Doppler blood flow imaging, Masson trichrome staining, and survival area analysis were used to assess the viability of the flaps. Apoptosis, Ferroptosis, oxidative stress, angiogenesis, and the underlying mechanisms were explored by examining the expression of specific molecules using immunofluorescence, western blotting, and Other immunological and Molecular Biology techniques. The findings demonstrated that MaR1 could improve FLAP lifespan by significantly reducing oxidative stress, Apoptosis, and Ferroptosis, as well as by enhancing angiogenesis. The Keap1-Nrf2 pathway was upregulated by MaR1, which inhibited ROS-mediated Apoptosis and Ferroptosis. The protective effect of MaR1 on FLAP survival was abolished by ML385. Our findings indicate that MaR1 could be a novel therapeutic agent for enhancing FLAP treatment outcomes.

Keywords

Ferroptosis; Keap1/Nrf2 signaling pathway; Maresin 1; ROS; Random skin flap.

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