Natural Astaxanthin-Loaded Hyaluronic Acid Hydrogel Promotes Full-Thickness Wound Repair by Inhibiting NF-κB...

BackgroundThe maintenance of physiological homeostasis in the human body depends on healthy skin, making optimal wound treatment crucial. In this study, a natural bioactive wound dressing combining astaxanthin and a hyaluronic acid hydrogel was developed.MethodsMice with full-thickness skin wounds were divided into different groups: the untreated control group, the blank hyaluronic acid hydrogel group, the polyethylene glycol hyaluronic acid hydrogel group, and the 2%, 4%, and 8% astaxanthin-hyaluronic acid hydrogel groups. The wound healing process was evaluated by observing the general view of the wound and collecting skin samples for HE and Masson staining. The mRNA expression levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) in the wound tissue were analysed via qRT-PCR. The protein expression levels of collagen I, CD31, α-SMA, Nrf2, HO-1, and NF-κB were examined through Western blot analysis. Additionally, the levels of oxidative stress-related indicators (MDA and SOD) were quantified.ResultsCompared with other hydrogels, ATX@HA gels accelerated full-thickness wound healing, promoting faster wound contraction. These gels enhanced vascularization, as shown by increased CD31 and α-SMA protein expression and increased granulation tissue formation. The ATX@HA gels improved collagen deposition, with a more regular arrangement of collagen fibres in the treated wounds. They reduced oxidative stress (lower MDA and higher SOD) and inflammation (less IL-1β and IL-6 and more IL-10). ATX@HA gels inhibited NF-κB activation and activated the Nrf2/HO-1 signalling pathway during wound healing.ConclusionsATX@HA has a therapeutic effect on wounds by enhancing vascularization and facilitating orderly collagen formation at the wound site while exerting anti-inflammatory and antioxidant effects. Further investigation revealed that these effects may be attributed to the inhibition of NF-κB activation and promotion of Nrf2/HO-1 pathway activation.