Astaxanthin Attenuates Early Acute Kidney Injury Following Severe Burns in Rats by Ameliorating Oxidative Stress and Mitochondrial-Related Apoptosis

Marine Drugs

Song-Xue Guo³  Han-Lei Zhou³  Chun-Lan Huang²  Chuan-Gang You³  Quan Fang¹  Pan Wu³  Xin-Gang Wang³  Chun-Mao Han³ 

[1] Department of Plastic Surgery, Binjiang Branch, Second Affiliated Hospital, School of Medicine, Zhejiang University, 1511 Jianghong Road, Hangzhou 310000, Zhejiang, China; E-Mail:;Department of Plastic Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, 79 Qingchun Road, Hangzhou 310000, Zhejiang, China; E-Mail:;Department of Burns, Second Affiliated Hospital, School of Medicine, Zhejiang University, 88 Jiefang Road, Hangzhou 310009, Zhejiang, China; E-Mails:

关键词: astaxanthin;    acute kidney injury;    burn;    oxidative stress;    apoptosis;    mitochondria;   

DOI  :  10.3390/md13042105

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.