In:
Nephron Experimental Nephrology, S. Karger AG, Vol. 128, No. 1-2 ( 2014-10-31), p. 37-45
Abstract:
〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 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. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 We used an IL-10 〈 sup 〉 -/- 〈 /sup 〉 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. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 There was a greater increase in serum creatinine in IL-10 〈 sup 〉 -/- 〈 /sup 〉 mice than in wild-type (WT) mice. And compared with WT mice, IL-10 〈 sup 〉 -/- 〈 /sup 〉 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 〈 sup 〉 -/- 〈 /sup 〉 mice compared with the WT mice. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 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.
Type of Medium:
Online Resource
ISSN:
1660-2129
Language:
English
Publisher:
S. Karger AG
Publication Date:
2014
detail.hit.zdb_id:
2098337-2
