期刊
AMERICAN JOURNAL OF NEPHROLOGY
卷 40, 期 5, 页码 441-450出版社
KARGER
DOI: 10.1159/000369220
关键词
Mangiferin; Sepsis-induced acute kidney injury; Nrf2; NLRP3
资金
- National Natural Science Foundation of China [81400721, 81373227, 81170663]
- Department of Nephrology
- National Key Clinical Specialty Construction Project of China
- National Key Technology RD Program [2011BAI10B08]
Background: Acute kidney injury (AKI) is a frequent and serious complication of sepsis. A growing body of evidence now suggests that inflammatory reactions and tubular dysfunction induced by oxidative stress involved in the mechanisms of the disease. This study aimed to determine the role of anti-inflammatory and anti-oxidant activities of mangiferin (MA) in sepsis-induced AKI. Methods: We investigated the effects of MA on apoptosis of rat kidney proximal tubular cell (RPTC), together with renal function and morphological alterations of mice undergoing cecal-ligation and puncture (CLP). The levels of oxidative stress in kidney tissues were also determined. Moreover, we mainly focus on the effects of MA in regulating the production of NLRP3 and Nrf2 in the present study. Results: The exposure to LPS (5 mu g/ml) yielded a significant increase of apoptosis in RPTC cells, which was largely inhibited by MA pretreatment. MA attenuates renal dysfunction and ameliorates the morphological changes in the septic mice induced by CLP. MA inhibits oxidative stress, decreases serum levels of IL-1 beta and IL-18, and prevents tubular epithelial cells apoptosis in kidneys of CLP mice model. Data in this study also suggest that MA promotes Nrf2 expression and suppresses renal NLRP3 inflammasome activation. Conclusion: In summary, MA protects against sepsisinduced AKI through NLRP3 inflammasome inhibition and Nrf2 up-regulation. Thus, the mangiferin could thus be a promising candidate for development of a multi-potent drug. (C) 2014 S. Karger AG, Basel
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