Mechanisms of Nrf2 and NF-κB pathways in diabetic wound and potential treatment strategies

Abstract

The issue of delayed wound healing or nonhealing in diabetic patients presents a challenge for modern medicine. A number of attempts have been made to understand the mechanisms behind diabetic wound. In a hyperglycemic environment, increased intracellular reactive oxygen species (ROS) disturb the balance between oxidation and antioxidant, causing the wound environment to deteriorate. It has been established that the nuclear factor E2-related factor 2 (Nrf2) and nuclear factor-kappa B (NF-κB) pathways play an important role in regulating in ammation and oxidative stress. Several potential treatment strategies involving Nrf2 and/or NF-κB pathways have been explored in previous studies. Hence, we analyzed mechanisms and changes in Nrf2 and NF-κB pathways in response to oxidative stress and in ammation in diabetic environment. Additionally, we reviewed potential treatment strategies from the past ve years for diabetic wound by Nrf2 and/or NF-κB pathways, including receptor agonists, vitamins, hormones, exosomes, drugs, plants, and biomaterials. It may be useful to develop drugs to promote diabetic wound healing.

Hyaluronidase‐Responsive Bactericidal Cryogel for Promoting Healing of Infected Wounds: Inflammatory Attenuation, ROS Scavenging, and Immune Regulation

“…NF‐κb1 is a crucial transcription factor that modulates inflammatory response and oxidative stress, activating the NF‐κB signaling pathway to induce the polarization of macrophages toward M1 type. [ 40 , 41 , 42 ] Thus, the HA/TA2/KR2 treatment could reduce inflammation and oxidative stress by inhibiting NF‐κB signaling pathway, and promote the polarization of macrophages toward M2 type to an extent. More importantly, we also observed that both the key protein Stat6 and the signaling pathway of JAK‐STAT6 that mediated M2 type macrophages polarization were upregulated in the HA/TA2/KR2 group.…”