Abstract:
Impaired wound healing in diabetic patients is a major clinical challenge, often associated
with mitochondrial dysfunction, increased inflammation, and oxidative stress. Trisk95, a
transmembrane protein, plays a critical role in calcium homeostasis, and its modulation
may enhance wound repair processes. Benfotiamine, a thiamine derivative, improves
diabetic complications by affecting oxidative stress, inflammation, metabolism, and
signaling pathways. This study aimed to evaluate the efficacy of benfotiamine in diabetic
wound healing by impacting Trisk95 expression and exerting anti-inflammatory and
antioxidant effects. Benfotiamine was administered topically to the wounded area of
diabetic mice and the wound closure rate was measured. The anti-inflammatory effects
were quantified by measuring interleukin-6 (IL-6) and interleukin-10 (IL-10) levels.
Antioxidant effects were assessed by measuring reactive oxygen species (ROS) level, and
the activity of superoxide dismutase (SOD) and catalase (Cat). Benfotiamine significantly
downregulated Trisk95, IL-6, and ROS levels, and upregulated IL-10. It increased the
activity of SOD and Cat enzymes. In conclusion, benfotiamine promotes wound healing in
diabetic mice by modulating Trisk95 and exerting anti-inflammatory and antioxidant
effects, thereby improving mitochondrial function.
Keywords: Trisk95, diabetic wound heali
