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Proteomic alterations in mouse kidney induced by andrographolide sodium bisulfite

文献类型： 外文期刊

作者： Lu, Hong 1 ; Zhang, Xin-yue 2 ; Zhou, Yan-quan 1 ; Wen, Xin 4 ; Zhu, Li-ying 3 ;

作者机构： 1.Zhejiang Chinese Med Univ, Sch Pharmacol, Hangzhou 310053, Zhejiang, Peoples R China

2.Zhejiang Chinese Med Univ, Inst Mat Med, Hangzhou 310013, Zhejiang, Peoples R China

3.Zhejiang Acad Agr Sci, Inst Plant Protect & Microbiol, State Key Lab Breeding Base Zhejiang Sustainable, Hangzhou 310021, Zhejiang, Peoples R China

4.Univ So Calif, Sch Dent, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA

关键词： andrographolide sodium bisulfite;Lianbizhi injection;nephrotoxicity;proteomics;reactive oxygen species;peroxiredoxin-6

期刊名称：ACTA PHARMACOLOGICA SINICA （ 影响因子：6.15； 五年影响因子：6.123 ）

ISSN： 1671-4083

年卷期： 2011 年 32 卷 7 期

页码：

收录情况： SCI

摘要： Aim: To identify the key proteins involved in the nephrotoxicity induced by andrographolide sodium bisulfite (ASB). Methods: Male ICR mice were intravenously administrated with ASB (1000 or 150 mg.kg(-1).d(-1)) for 7 d. The level of malondialdehyde (MDA) and the specific activity of superoxide dismutase (SOD) in kidneys were measured. The renal homogenates were separated by two-dimensional electrophoresis, and the differential protein spots were identified using a matrix-assisted laser desorption/ionization (MALDI) time-of-flight (TOF)/TOF mass spectrometry. Results: The high dose (1000 mg/kg) of ASB significantly increased the MDA content, but decreased the SOD activity as compared to the control mice. The proteomic analysis revealed that 6 proteins were differentially expressed in the high-dose group. Two stress-responsive proteins, ie heat shock cognate 71 kDa protein (HSC70) and peroxiredoxin-6 (PRDX6), were regulated at the expression level. The remaining 4 proteins involving in cellular energy metabolism, including isoforms of methylmalonyl-coenzyme A mutase (MUT), nucleoside diphosphate-linked moiety X motif 19 (Nudix motif19), mitochondrial NADH dehydrogenase 1 alpha subcomplex subunit 10 (NDUFA10) and nucleoside diphosphate kinase B (NDK B), were modified at the post-translational levels. Conclusion: Our findings suggest that the mitochondrion is the primary target of ASB and that ASB-induced nephrotoxicity results from oxidative stress mediated by superoxide produced by complex I.

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