Figure 10.

Schematic diagram illustrating of the potential mechanism of HB-mediated diabetic wound healing. Reactive oxygen species in diabetic wound caused DNA double strands breakage, lipid peroxide, protein denaturation, and impaired diabetic wound healing. Specifically, Nrf2 and its downstream antioxidant genes were significantly decreased, and wound healing was impaired. In contrast, HB liniment markedly increased Nrf2 level and its downstream genes involved in GSH- and Trx-based systems, NADPH generation, and other antioxidant systems; this led to enhanced antioxidant capacity and decreased oxidative and apoptosis damage. Additionally, these also increased TGF-β1 and collagen growth while decreased MMP9, which accelerated wound closure in HB-mediated wound healing.