Pretreatment with Glutamine Attenuates Anoxia/Reoxygenation Injury of Human Proximal Renal Tubular Epithelial Cells via Induction of Heme Oxygenase-1

被引:13
|
作者
Shi, Qiang [1 ]
Feng, Ya-Ni [2 ]
Fang, Jun [3 ]
Xu, Ke [1 ]
机构
[1] China Med Univ, Affiliated Hosp 1, Dept Radiol, Shenyang 110005, Peoples R China
[2] China Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Shenyang 110005, Peoples R China
[3] Sojo Univ, Fac Pharmaceut Sci, Lab Microbiol & Oncol, Kumamoto, Japan
关键词
Glutamine; Heme oxygenase-1; Apoptosis; Anoxia/reoxygenation; Ischemia/reperfusion; HEAT-SHOCK-PROTEIN; NITRIC-OXIDE; KINASE PATHWAYS; APOPTOSIS; ISCHEMIA; ACTIVATION; EXPRESSION; PROTECTION; GENE; LUNG;
D O I
10.1159/000220767
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background/Aims: Glutamine showed potential cytoprotective activity probably due to induction of heme oxygenase-1 (HO-1). We thus investigated the effect of glutamine in vitro on anoxia/reoxygenation (A/R) injury of renal tubular epithelial cells. Methods: Human proximal renal tubular epithelial cells (HK-2) were subjected to A/R with or without glutamine, after which viability and apoptosis of the cells were determined by MTT assay and annexin V flow cytometry, respectively. Meanwhile, expression of HO-1, caspase-3, Bcl-2 and inducible nitric oxide synthetase (iNOS) was measured by reverse transcriptase polymerase chain reaction and Western blot. Results: A/R significantly induced apoptosis of HK-2 cells, which was inhibited by glutamine, during which HO-1 was upregulated significantly, but nullified by p38MAPK inhibitor. Caspase-3 and iNOS increased after A/R; however, glutamine inhibited this potential. Opposite results were observed for Bcl-2. Conclusion: Glutamine prevents A/R injury of HK-2 cells through induction of HO-1 via a p38MAPK-dependent pathway, which plays a key role in the cytoprotective effect of glutamine. Copyright (C) 2009 S. Karger AG, Basel
引用
收藏
页码:1 / 8
页数:8
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