Literature DB >> 25376659

IL-10 deficiency increases renal ischemia-reperfusion injury.

Xin Wan1, Wen Juan Huang, Wen Chen, Hong-Guang Xie, Pan Wei, Xin Chen, Chang-Chun Cao.   

Abstract

BACKGROUND: Renal ischemia-reperfusion (IR) injury is a frequent cause of acute kidney injury, which results in high morbidity and mortality. Inflammation is an important factor that is involved in kidney repair after renal IR injury. IL-10 is a potent anti-inflammatory cytokine that inhibits inflammatory pathways, but the role of IL-10 in repairing renal IR injury is not known. Here, we investigated the role of IL-10 in kidney repair after renal IR injury.
METHODS: We used an IL-10(-/-) mouse model and examined the serologic and histomorphology of kidney after IR injury. We also measured ki67, TNF-α, IL-6, and macrophages with immunohistochemistry or Western blotting.
RESULTS: There was a greater increase in serum creatinine in IL-10(-/-) mice than in wild-type (WT) mice. And compared with WT mice, IL-10(-/-) mice had increased histologic renal injury and decreased proliferation. Moreover, the expression of TNF-α, IL-6 and macrophages was clearly increased in IL-10(-/-) mice compared with the WT mice.
CONCLUSION: These data reveal an important role for IL-10 in the improvement of renal IR injury, acting through suppression of inflammatory mediators, and that IL-10 would be a crucial target for the treatment of IR injury.
© 2014 S. Karger AG, Basel.

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Year:  2014        PMID: 25376659     DOI: 10.1159/000366130

Source DB:  PubMed          Journal:  Nephron Exp Nephrol        ISSN: 1660-2129


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