Abstract
Early acute kidney injury (AKI) is a devastating complication in critical burn patients, and it is associated with severe morbidity and mortality. The mechanism of AKI is multifactorial. Astaxanthin (ATX) is a natural compound that is widely distributed in marine organisms; it is a strong antioxidant and exhibits other biological effects that have been well studied in various traumatic injuries and diseases. Hence, we attempted to explore the potential protection of ATX against early post burn AKI and its possible mechanisms of action. The classic severe burn rat model was utilized for the histological and biochemical assessments of the therapeutic value and mechanisms of action of ATX. Upon ATX treatment, renal tubular injury and the levels of serum creatinine and neutrophil gelatinase-associated lipocalin were improved. Furthermore, relief of oxidative stress and tubular apoptosis in rat kidneys post burn was also observed. Additionally, ATX administration increased Akt and Bad phosphorylation and further down-regulated the expression of other downstream pro-apoptotic proteins (cytochrome c and caspase-3/9); these effects were reversed by the PI3K inhibitor LY294002. Moreover, the protective effect of ATX presents a dose-dependent enhancement. The data above suggested that ATX protects against early AKI following severe burns in rats, which was attributed to its ability to ameliorate oxidative stress and inhibit apoptosis by modulating the mitochondrial-apoptotic pathway, regarded as the Akt/Bad/Caspases signalling cascade.
Highlights
Acute kidney injury (AKI) is a major common and devastating complication in severely burned patients (total body surface area (TBSA) ≥20%)
The tubular damage scores significantly increased in the burn and burn + vehicle groups at 24 h post burn, whereas the levels of serum creatinine (Cr) and neutrophil gelatinase-associated lipocalin (NGAL)
With ATX administration, the 20 mg/kg group presented a significant decrease in the tubular damage score, compared with burn groups, the tubular damage score in the 5 mg/kg and 10 m/kg groups declined slightly (Figure 1B)
Summary
Acute kidney injury (AKI) is a major common and devastating complication in severely burned patients (total body surface area (TBSA) ≥20%). AKI may be attributed to intravascular hypovolaemia, systemic vasoconstriction, early organ dysfunction or myoglobinuria, resulting from oxidative stress or apoptosis [6,7,8]. ROS-mediated oxidative stress is involved in the development of renal dysfunction followed by AKI or other diseases, which may result in disruptions in cellular functions and induced mitochondrial-related apoptosis via various free radicals [16,17]. Based on increased research evidence, early and timely interventions for oxidative stress and secondary apoptosis in renal tissue may present a potential protective avenue for severe burn-induced AKI [18]
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