Abstract
Cellular metabolism is a key regulator of tissue repair and regeneration, with mitochondrial function playing a central role in energy production and cellular homeostasis. Dysfunctional mitochondria, often due to excessive reactive oxygen species (ROS), contribute to oxidative stress, impaired wound healing, and chronic inflammation. This study investigates the therapeutic potential of DeepA-I, a Boron-enriched compound, in enhancing mitochondrial health, reducing oxidative damage, and promoting cellular repair in human umbilical vein endothelial cells (HUVEC) and mouse embryonic fibroblasts (MEF). Boron quantification via inductively coupled plasma optical emission spectroscopy (ICP-OES) confirmed its presence in DeepA-I. Cytotoxicity assessment (MTT assay) demonstrated its safety, while fluorescence microscopy (DAPI, MitoSPY, DCFDA) revealed reduced ROS levels and preserved mitochondrial integrity. A scratch assay showed accelerated cell migration and wound closure in DeepA-I-treated cells. Western blot analysis indicated the downregulation of Akt (a proliferation marker) and the upregulation of NRF2, a key regulator of oxidative stress resistance, without affecting apoptosis-related proteins. These results suggest that DeepA-I, via its Boron-mediated mechanisms, enhances mitochondrial function, mitigates ROS-induced damage, and improves tissue repair, positioning it as a promising therapeutic candidate for inflammatory and degenerative conditions.