The Protective Role of Strong Antioxidant Astaxanthin on Burn Wound and Burn-Induced Early Acute Kidney Injury through Abilities to Relieve Oxidative Stress and Inhibit Apoptosis by Modulating Mitochondrial-Apoptotic Pathways

Summary: Burns are skin damage caused by heat trauma or cold trauma (frost bite). Causes include fire, hot water, electricity, chemicals, radiation, and cold (frostbite). This damage may involve subcutaneous tissue. Burn injuries are associated with high incidence and prevalence, high risk of morbidity and mortality, resource-intensive, and costly. One of the most common complications in burn patients is acute kidney injury (AKI). The mechanism of early AKI after burn injury is multifactorial, and previous studies have mainly focused on oxidative stress injury, tubular apoptosis, and systemic or local inflammation. Previous results (from our group and others) suggested that ROS-induced oxidative stress damage and apoptosis play an important role in the development of early AKI due to burn injury, and that 24 h after burn injury are useful for observing changes in burn injury. It shows that it provides an important timeframe. Kidney function and levels of oxidative stress and apoptosis. Astaxanthin (ATX) is a naturally occurring carotenoid that is readily obtained from marine organisms and stronger antioxidant effects than other carotenoids. Given the critical role of oxidative stress and secondary renal inflammation in severe burn-induced early AKI, a protective role of ATX through its anti-inflammatory effects and potential mechanisms of action in early post-burn AKI is reasonable.