RGD Reference Report - Ischemic preconditioning attenuates renal ischemia-reperfusion injury by inhibiting activation of IKKbeta and inflammatory response. - Rat Genome Database

RGD Reference Report - Ischemic preconditioning attenuates renal ischemia-reperfusion injury by inhibiting activation of IKKbeta and inflammatory response. - Rat Genome Database

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Ischemic preconditioning attenuates renal ischemia-reperfusion injury by inhibiting activation of IKKbeta and inflammatory response.
Authors:	Chen, X Liu, X Wan, X Wu, Y Chen, Y Cao, C
Citation:	Chen X, etal., Am J Nephrol. 2009;30(3):287-94. doi: 10.1159/000225928. Epub 2009 Jun 16.
RGD ID:	7495779
Pubmed:	PMID:19546526 (View Abstract at PubMed)
DOI:	DOI:10.1159/000225928 (Journal Full-text)
BACKGROUND: Renal ischemia-reperfusion (I/R) injury is a major cause of acute renal failure (ARF). The transcription factor nuclear factor-kappaB (NF-kappaB) has been implicated as a key mediator of reperfusion injury. Activation of NF-kappaB is dependent upon the phosphorylation of its inhibitor, IkappaB, by the specific inhibitory kappaB kinase (IKK) subunit, IKKbeta. We hypothesized that ischemic preconditioning (IPC) reduces acute renal damage following I/R injury by inhibiting activation of IKKbeta. As neutrophil gelatinase-associated lipocalin (NGAL), an early predictive biomarker of acute kidney injury, is regulated by NF-kappaB, we approached the relationship between NGAL and IKKbeta. METHOD: Thirty male Sprague-Dawley rats were randomly divided into 3 groups after right kidney nephrectomy. Group A rats were sham-operated controls. Group B rats were 45-min ischemic in the left renal artery while Group C rats were pre-treated with 3 cycles of 2-min ischemia and 5-min reperfusion. All the rats were sacrificed at 24 h after reperfusion. We harvested kidneys and serum to do further analysis, including histological and functional parameters, expressions of NGAL and IKKbeta in renal tissues. RESULTS: Compared with rats subjected to I/R injury, pre-treated rats had a significant decrease in serum creatinine level (Scr) and tubulointerstitial injury scores (Scr, 86.79 +/- 12.98 vs. 205.89 +/- 19.16 mircomol/l, p < 0.01; tubulointerstitial injury scores, 1.3 +/- 0.48 vs. 3.8 +/- 0.79, p < 0.01). In addition, expressions of IKKbeta (0.95 +/- 0.21 vs. 1.74 +/- 0.17, p < 0.05) and NGAL (1.71 +/- 0.032 vs. 2.66 +/- 0.078, p < 0.05) at renal tubule in pre-treated rats were attenuated significantly compared with rats subjected to ischemia-reperfusion injury. Moreover, our study showed that IKKbeta and NGAL were in positive correlation (R = 0.965 > R(0.01)(30) = 0.448, p < 0.01). CONCLUSIONS: The evidence suggests that IKKbeta may play a role in renal I/R injury and give rise to the generation of NGAL. It appears that IPC may attenuate renal injury and the expression of NGAL following acute I/R injury. IKKbeta may offer a clinically accessible target for preventing renal injury following I/R.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
IKBKB	Human	Kidney Reperfusion Injury	treatment	ISO	Ikbkb (Rattus norvegicus)		RGD
Ikbkb	Rat	Kidney Reperfusion Injury	treatment	IMP			RGD
Ikbkb	Mouse	Kidney Reperfusion Injury	treatment	ISO	Ikbkb (Rattus norvegicus)		RGD

Genes (Rattus norvegicus)


Ikbkb (inhibitor of nuclear factor kappa B kinase subunit beta)

Genes (Mus musculus)


Ikbkb (inhibitor of kappaB kinase beta)

Genes (Homo sapiens)


IKBKB (inhibitor of nuclear factor kappa B kinase subunit beta)