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2015 ; 8
(10
): 13114-9
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Sevoflurane pretreatment enhance HIF-2? expression in mice after renal
ischemia/reperfusion injury
#MMPMID26722509
Zheng B
; Zhan Q
; Chen J
; Xu H
; He Z
Int J Clin Exp Pathol
2015[]; 8
(10
): 13114-9
PMID26722509
show ga
Ischemia/reperfusion (I/R) injury often occurs, which is one of the major causes
of acute kidney injury, thus increasing in-hospital mortality. HIF-2? has a
protective role against ischemia of the kidney. Renal ischemia/reperfusion under
sevoflurane anesthesia resulted in drastic improvements in renal function. We
hypothesized that underlying mechanism responsible for renal protection from
sevoflurane pretreatment involves the upregulation of HIF-2?. Sevoflurane
pretreatment were performed on WT and HIF-2? knockout mice before renal
ischemia/reperfusion. Levels of blood urea nitrogen (BUN) and serum creatinine
(Cr) were determined with a standard clinical automatic analyzer. The left
kidneys were taken for morphological examination. Expression of HIF-2? in kidney
tissue was examined by western blotting. In WT mice, group I/R injury had
significantly higher BUN and Cr levels than group control, whereas group I/R +
Sev had significantly lower BUN and Cr levels than group I/R injury. Renal HIF-2?
expression levels were significantly higher in WT mice of group I/R + Sev than
group control and group I/R. In HIF-2?(-/-) mice, group I/R + Sev showed much
higher BUN and Cr levels and severer histological damage than group I/R and group
control. Renal HIF-2? expression levels were significantly higher in WT mice of
group I/R + Sev than group control and group I/R. Our findings suggested that
HIF-2? might contribute to the beneficial effect of sevoflurane in renal
ischemia/reperfusion injury.