Protective Effects of Neutrophil Gelatinase–Associated Lipocalin on Hypoxia/Reoxygenation Injury of HK-2 Cells

Cui, Liyan; Yang, Shuo; Zhang, J.

doi:10.1016/j.transproceed.2011.08.090

Cited by 14 publications

(15 citation statements)

References 29 publications

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“…The acutephase glycoprotein LCN2 is active under inflammation, apoptosis, and suppression of bacterial growth. There is recent evidence that Lcn2 also has a pivotal role in the protection against oxidative stress during hypoxia/reoxygenation in vitro (30) and that it acts as an antioxidant (31). Still, we could not detect …”

Section: Hyperoxia-induced Transcriptional Changescontrasting

confidence: 61%

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

et al. 2013

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Section: Hyperoxia-induced Transcriptional Changescontrasting

confidence: 61%

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

et al. 2013

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“…9,10 In vitro experiments also confirmed that exogenous NGAL could inhibit the apoptosis of HK-2 cells, which suffered hypoxia (1 h) and reoxygenation (24 h). 24 Thus, we assumed that NGAL may play a role in renal protection via inhibiting the apoptosis of renal tubular epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…One experiment in vitro also showed that exogenous NGAL could reduce the level of Bax/Bcl-2 mRNA in HK-2 cells, which suffered hypoxia and reoxygenation. 24 So we assumed that the renoprotection effect of NGAL was achieved mainly by inhibiting the activation of caspase-3, reducing the expression of Bax, and thus inhibiting cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin (NGAL) May Play a Protective Role Against Rats Ischemia/Reperfusion Renal Injury via Inhibiting Tubular Epithelial Cell Apoptosis

Zang

Wang

et al. 2012

Renal Failure

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We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) on rats ischemia/reperfusion (I/R) renal injury. Eighteen Sprague-Dawley male rats were randomly divided into three groups. Control group (n ¼ 6) suffered left unilateral nephrectomy, I/R þ NS (normal saline) (n ¼ 6) and I/R þ NGAL (n ¼ 6) group were subjected to 45 min right renal ischemia/24 h reperfusion after left unilateral nephrectomy. Serum creatinine (Scr) and blood urea nitrogen (Bun) were measured on automatic biochemistry analyzer; kidney sections were stained with hematoxylin-eosin; terminal dUTP nick-labeling method was used to examine the apoptosis of tubular epithelial cells; Cleaved caspase-3 and Bax protein expression were detected by immunohistochemistry and Western Blot; real-time polymerase chain reaction was used to detect the expression of Bax mRNA. Rats with NGAL displayed an attenuated renal damage and a decreased number of tubular epithelial cell apoptosis compared to the I/R þ NS group (Scr 63.400 AE 11.908 vs. 121.857 AE 17.151 μmol/L, Bun 14.840 AE 2.868 vs. 28.557 AE 6.434 mmol/L, apoptosis cell number 7.800 AE 1.924 vs. 15.400 AE 3.049/high power field (HPF), p < 0.05), the values were lower in the control group (24.000 AE 3.829 μmol/L, 5.814 AE 1.961 mmol/L, 1.800 AE 0.837/HPF, p < 0.05) compared to two groups above; NGALtreated rats showed down-regulated Cleaved caspase-3 protein (0.284 AE 0.066 vs. 0.409 AE 0.073, p < 0.05), Bax protein (0.346 AE 0.055 vs. 0.443 AE 0.041, p < 0.05), Bax mRNA (1.423 AE 0.187 vs. 2.550 AE 0.217, p < 0.05) compared to I/R þ NS group, but the values were higher in both of the two groups than those in the control group (Cleaved caspase-3 protein 0.104 AE 0.029, Bax protein 0.155 AE 0.027, Bax mRNA 1.000 AE 0.000, p < 0.05). We supposed that exogenous NGAL can inhibit the activation of caspase-3, reduce the expression of Bax, and thus reduce renal tubular cell apoptosis and protect renal function in I/R injury rats.

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“…Compared with I/R group, the expression of Fas mRNA in renal tubular epithelial cells of the NGAL group declined, while the expression of Bcl-2 mRNA increased, showing significant differences, indicating that NGAL may have renoprotective activity by reducing the expression of Fas and enhancing the expression of Bcl-2, thereby inhibiting the occurrence of apoptosis. In vitro experiments also proved that NGAL could inhibit the apoptosis of HK-2 cells subjected to hypoxia and reoxygenation (Cui et al, 2011).…”

Section: Discussionmentioning

confidence: 85%

In vivo mechanism study of NGAL in rat renal ischemia-reperfusion injury

Zang

Zhang

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to determine the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) in rat kidney on ischemia/reperfusion injury (I/R). The rat I/R model was set up by cutting one kidney and clamping the contralateral renal pedicle for 45 min. Male SD rats were randomly divided into sham-operation, I/R and NGAL groups. Hematoxylin-eosin staining was performed to observe the renal pathological changes in the 3 groups; serum creatinine (Scr) and blood urea nitrogen (BUN) determined in blood samples taken from the inferior vena cava 24 h after the reperfusion were measured; TUNEL was used to observe the apoptosis of renal tubular epithelial cells; immunohistochemistry was performed to evaluate the expressions of Bax and activated caspase-3; Western blotting was used to determine the expression changes in apoptotic proteins Fas and Bcl-2. Compared with the I/R group, Scr and BUN of the NGAL group were 63.400 ± 11.908 vs 121.857 ± 17.151 µM and 14.840 ± 2.868 vs 28.557 ± 6.434 mM, respectively. The number of apoptotic tubular epithelial cells was reduced (7.800 ± 1.924 vs 15.400 ± 3.049); the expression of 8741 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 13 (4): 8740-8748 (2014) Study of NGAL in renal ischemia-reperfusion injury renal tissue Fas mRNA of the NGAL group was decreased (2.34 ± 0.51 vs 6.84 ± 2.34); the expression of the Bax protein was lower (7.440 ± 1.640 vs 15.456 ± 1.955%); the expression of the CC3 protein was decreased (3.171 ± 0.321 vs 7.291 ± 1.059%), while the expression of the Bcl-2 protein increased (6.91 ± 1.64 vs 5.30 ± 1.48), P < 0.05. NGAL had a protective effect towards the renal tubular epithelial cells in I/R, and the effect might have been associated with the reduction in apoptosis and the altered expression of apoptotic proteins, which would thereby reduce tissue damage and protect the kidney.

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Protective Effects of Neutrophil Gelatinase–Associated Lipocalin on Hypoxia/Reoxygenation Injury of HK-2 Cells

Cited by 14 publications

References 29 publications

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

Neutrophil Gelatinase-Associated Lipocalin (NGAL) May Play a Protective Role Against Rats Ischemia/Reperfusion Renal Injury via Inhibiting Tubular Epithelial Cell Apoptosis

In vivo mechanism study of NGAL in rat renal ischemia-reperfusion injury

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