Benfotiamine prevents endotoxin-induced cytotoxicity in human dermal fibroblasts

Summary: Abstract Body: Wound healing is a fundamental physiological process involving a complex cascade of cellular events that repair damaged tissue. Impairments in wound healing mechanisms, often exacerbated by conditions such as diabetes, infections, and oxidative stress, highlight the need for novel therapeutic strategies. Oxidative stress, marked by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, can significantly hinder the repair process. This study investigates the therapeutic potential of benfotiamine, a lipophilic derivative of thiamine (vitamin B1), in preventing lipopolysaccharides (LPS) induced human dermal fibroblasts (HDFs) apoptosis. Benfotiamine is known for its ability to increase thiamine levels in tissues and exert antioxidative effects, thereby potentially countering oxidative stress and its detrimental effects on wound healing. Our study utilizes LPS to induce oxidative stress in HDFs and examined how vitamin B1 derivative counters this. HDFs were treated with LPS in the absence or presence of various concentrations of benfotiamine, and cell viability was assessed. Preliminary results show that cells treated with benfotiamine prevented LPS-induced decrease by 15% (p=0.001) in cell viability. These findings suggest that benfotiamine may mitigate oxidative stress-induced cytotoxicity and apoptosis in HDFs. Future experiments will explore benfotiamine’s effects on apoptotic signaling by examining caspase-3 activation, PARP cleavage, and the expression of apoptotic markers. Additional in-vivo studies are planned to determine the therapeutic potential of benfotiamine in improving wound healing. Mindy Huynh¹, Zackery Paxton¹ 1. Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT, United States. Stem Cell Biology, Tissue Regeneration and Wound Healing