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Int Urol Nephrol. 2019 Feb;51(2):351-358. doi: 10.1007/s11255-018-2027-2. Epub 2018 Nov 19.

Protective effect of astaxanthin against contrast-induced acute kidney injury via SIRT1-p53 pathway in rats.

Author information

1
Institute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, 221002, Jiangsu, China.
2
Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, No.99 Huaihai West Road, Xuzhou, 221002, Jiangsu, China.
3
Institute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, 221002, Jiangsu, China. xzwenhua0202@163.com.
4
Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, No.99 Huaihai West Road, Xuzhou, 221002, Jiangsu, China. xzwenhua0202@163.com.

Abstract

PURPOSE:

The present study was designed to further investigate the protective effect of astaxanthin (AST) on contrast-induced acute kidney injury (CI-AKI) in rats and the relationship between SIRT1-p53 pathway and astaxanthin.

METHODS:

40 adult male Sprague Dawley (SD) rats were randomly divided into five groups (n = 8/group): control (CON), normal rats treated with AST (AST), CM-treated (CM), CM rats treated with isoform of nitric oxide synthase (iNOS) inhibitor (iNOS + CM), and CM rats treated with AST (AST + CM). Serum creatinine (Scr) and blood urea nitrogen (BUN) values were measured at 72 h following the procedure. Hematoxylin and eosin (H-E) staining was used to observe the pathologic changes of kidney. Tunel staining was used to test apoptosis of kidney tubules. Oxidative stress, SIRT1 activity, nitric oxide (NO), and 3-nitrotyrosine (3-NT) content were individually measured with the commercial available kits.

RESULTS:

Compared with the CON group, Scr and BUN levels significantly increased in the CM group (P < 0.05), and the values in two pre-treatment groups (iNOS + CM and AST + CM) had significantly decreased (P < 0.05). H-E and Tunel staining had shown that renal tubular injury was severe in CM group. The renal injury score and apoptosis index in the two pre-treatment groups also decreased (P < 0.05). The present study showed that in CM group the levels of oxidative stress indicators significantly increased, and the activities of antioxidant stress indicators significantly decreased. These indicators in two pre-treatment groups significantly improved (P < 0.05). In the CM group the expression levels of SITR1 significantly increased, and the ac-p53/p53 significantly increased (P < 0.05). Compared with the CM group, in AST + CM group the expression levels of SIRT1 increased, the expression levels of p53 and ac-p53/p53 decreased (P < 0.05).The levels of NO and 3-NT in CM group significantly increased (P < 0.05). Compared the CM group, the levels in the two pre-treatment groups significantly decreased (P < 0.05).

CONCLUSIONS:

Astaxanthin has a protective effect on CI-AKI, the mechanism may be related to the SIRT1-p53 pathway. Astaxanthin can reduce the content of NO and 3-NT in renal tissue of CI-AKI, and alleviate the renal injury induced by contrast agents.

KEYWORDS:

3-NT; Acute kidney injury; Apoptosis; Astaxanthin; Oxidative stress; SIRT1-p53 pathway

PMID:
30456546
DOI:
10.1007/s11255-018-2027-2

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