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本文引用的文献

1
Screening of herbal medicines for the recovery of cisplatin-induced nephrotoxicity.筛选草药以恢复顺铂诱导的肾毒性。
Environ Toxicol Pharmacol. 2009 Sep;28(2):206-12. doi: 10.1016/j.etap.2009.04.005. Epub 2009 Apr 15.
2
Attenuation of diabetic nephropathy by tocotrienol: involvement of NFkB signaling pathway.生育三烯酚对糖尿病肾病的缓解作用:NFkB信号通路的参与
Life Sci. 2009 Feb 27;84(9-10):296-301. doi: 10.1016/j.lfs.2008.12.014. Epub 2008 Dec 30.
3
The use of cultured primary bovine colon epithelial cells as a screening model to detect genotoxic effects of heterocyclic aromatic amines in the comet assay.
J Toxicol Environ Health A. 2008;71(13-14):947-53. doi: 10.1080/15287390801988962.
4
In vitro gene expression analysis of hepatotoxic drugs in rat primary hepatocytes.大鼠原代肝细胞中肝毒性药物的体外基因表达分析
J Appl Toxicol. 2008 Mar;28(2):227-36. doi: 10.1002/jat.1328.
5
Comparative analysis of gene expression between renal cortex and papilla in nedaplatin-induced nephrotoxicity in rats.奈达铂诱导大鼠肾毒性时肾皮质与肾乳头基因表达的比较分析。
Hum Exp Toxicol. 2007 Oct;26(10):767-80. doi: 10.1177/0960327107084069.
6
Cisplatin nephrotoxicity: a review.顺铂肾毒性:综述
Am J Med Sci. 2007 Aug;334(2):115-24. doi: 10.1097/MAJ.0b013e31812dfe1e.
7
Cisplatin induces mitochondrial oxidative stress with resultant energetic metabolism impairment, membrane rigidification and apoptosis in rat liver.顺铂可诱导大鼠肝脏产生线粒体氧化应激,进而导致能量代谢受损、膜僵化及细胞凋亡。
J Appl Toxicol. 2008 Apr;28(3):337-44. doi: 10.1002/jat.1284.
8
Cisplatin-induced acute renal failure is associated with an increase in the cytokines interleukin (IL)-1beta, IL-18, IL-6, and neutrophil infiltration in the kidney.顺铂诱导的急性肾衰竭与细胞因子白细胞介素(IL)-1β、IL-18、IL-6的增加以及肾脏中的中性粒细胞浸润有关。
J Pharmacol Exp Ther. 2007 Jul;322(1):8-15. doi: 10.1124/jpet.107.119792. Epub 2007 Mar 30.
9
Herbal medicine in the treatment of liver diseases.草药治疗肝脏疾病。
Dig Liver Dis. 2007 Apr;39(4):293-304. doi: 10.1016/j.dld.2006.11.004. Epub 2007 Feb 28.
10
Sesame oil attenuates Cisplatin-induced hepatic and renal injuries by inhibiting nitric oxide-associated lipid peroxidation in mice.芝麻油通过抑制小鼠体内一氧化氮相关的脂质过氧化作用减轻顺铂诱导的肝损伤和肾损伤。
Shock. 2007 Feb;27(2):199-204. doi: 10.1097/01.shk.0000238063.54332.06.

姜黄处理顺铂刺激的 HEK293 细胞的全基因组表达谱。

The genome-wide expression profile of Curcuma longa-treated cisplatin-stimulated HEK293 cells.

机构信息

Department of Physiology, College of Oriental Medicine Department of Oriental Pathology, College of Oriental Medicine, KyungHee University, Seoul 130-701, Republic of Korea.

出版信息

Br J Clin Pharmacol. 2010 Oct;70(4):547-56. doi: 10.1111/j.1365-2125.2010.03724.x.

DOI:10.1111/j.1365-2125.2010.03724.x
PMID:20840446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2950989/
Abstract

AIM

The rhizome of turmeric, Curcuma longa (CL), is a herbal medicine used in many traditional prescriptions. It has previously been shown that CL treatment showed greater than 47% recovery from cisplatin-induced cell damage in human kidney HEK 293 cells. This study was conducted to evaluate the recovery mechanisms of CL that occur during cisplatin induced nephrotoxicity by examining the genome wide mRNA expression profiles of HEK 293 -cells.

METHOD

Recovery mechanisms of CL that occur during cisplatin-induced nephrotoxicity were determined by microarray, real-time PCR, immunofluorescent confocal microscopy and Western blot analysis.

RESULTS

The results of microarray analysis and real-time PCR revealed that NFκB pathway-related genes and apoptosis-related genes were down-regulated in CL-treated HEK 293 cells. In addition, immunofluorescent confocal microscopy and Western blot analysis revealed that NFκB p65 nuclear translocation was inhibited in CL-treated HEK 293 cells. Therefore, the mechanism responsible for the effects of CL on HEK 293 cells is closely associated with regulation of the NFκB pathway.

CONCLUSION

CL possesses novel therapeutic agents that can be used for the prevention or treatment of cisplatin-induced renal disorders.

摘要

目的

姜黄的根茎,姜黄(CL),是一种草药,用于许多传统处方。先前已经表明,CL 治疗在人肾 HEK 293 细胞中显示出超过 47%的顺铂诱导的细胞损伤的恢复。本研究通过检查 HEK 293-细胞中顺铂诱导的肾毒性过程中的全基因组 mRNA 表达谱,评估 CL 在顺铂诱导的肾毒性过程中发生的恢复机制。

方法

通过微阵列、实时 PCR、免疫荧光共聚焦显微镜和 Western blot 分析确定 CL 在顺铂诱导的肾毒性过程中的恢复机制。

结果

微阵列分析和实时 PCR 的结果表明,CL 处理的 HEK 293 细胞中 NFκB 通路相关基因和凋亡相关基因下调。此外,免疫荧光共聚焦显微镜和 Western blot 分析表明,CL 处理的 HEK 293 细胞中 NFκB p65 核易位受到抑制。因此,CL 对 HEK 293 细胞的作用机制与 NFκB 通路的调节密切相关。

结论

CL 具有新的治疗剂,可用于预防或治疗顺铂诱导的肾脏疾病。