世界中医药
文章摘要
引用本文:吴胜斌,王应灯.人参皂苷20(s)-Rg3对llc-pk1细胞中顺铂所致肾毒性的保护作用[J].世界中医药,2018,(08):.  
人参皂苷20(s)-Rg3对llc-pk1细胞中顺铂所致肾毒性的保护作用
Protective Effects of Ginsenoside 20 (s)-Rg3 on Renal Toxicity Induced by Cisplatin in llc-pk1 Cells
投稿时间:2017-11-03  
DOI:10.3969/j.issn.1673-7202.2018.08.045
中文关键词:  顺铂  人参皂苷20(S)-Rg3  llc-pk1细胞  c-Jun N-末端激酶  肾毒性  发酵黑参  丝裂原活化蛋白激酶  细胞外调节蛋白激酶  磷酸脱氢酶  甘油醛-3-磷酸脱氢酶
English Keywords:Cisplatin  Ginsenoside 20 (S)-Rg3  llc-pk1 cell  c-Jun N-terminal kinase  Nephrotoxicity  FBG  MAPK  ERK  Phosphate dehydrogenase  Glyceraldehyde-3-phosphate dehydrogenase
基金项目:上海市自然科学基金项目(09ZR417400)
作者单位
吴胜斌,王应灯 上海交通大学医学院附属第九人民医院肾脏内科上海200011 
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中文摘要:
      目的:探讨人参皂苷20(s)-Rg3对llc-pk1细胞中顺铂所致肾毒性的保护作用。方法:通过基于细胞的肾脏保护试验,研究了发酵黑参(FBG)及其活性成分人参皂苷20(S)-Rg3对猪肾(LLC-PK1)细胞中顺铂(化疗药物)诱导的损伤的保护作用。结果:由顺铂诱导的细胞活力降低,再使用FBG提取物和人参皂苷20(S)-Rg3依赖剂量后明显恢复。用FBG提取物或人参皂苷20(S)-Rg3处理后会降低顺铂诱导升高与磷酸化c-Jun N-末端激酶(JNK),p53和裂解的半胱天冬酶-3升高的蛋白。通过用FBG和人参皂苷20(S)-Rg3的共同处理,由于顺铂的诱导导致凋亡LLC-PK1细胞升高的百分比显著降低。结论:人参皂苷20(s)-Rg3可改善LLC-PK1的细胞毒性,人参皂苷20(S)-RG3可能是通过阻断JNK-P53-caspase-3信号级联反应来介导这种作用的重要组成部分。
English Summary:
      To discuss protective effects of ginsenoside 20 (s)-Rg3 on renal toxicity induced by cisplatin in llc-pk1 cells. Methods:This article studied the protective effect of fermentation of black ginseng cells (FBG) and its active component ginsenoside 20 (S)-Rg3 on porcine kidney (LLC-PK1) cells in cisplatin (chemotherapy)-induced injury based on kidney protection test. Results:The cisplatin induced cell viability decreased, and then FBG was used to extract and ginsenoside 20 (S)-Rg3 was restored by FBG. After the dose dependent or extract ginsenoside 20 (S) after-Rg3 treatment may reduce cisplatin induced increased phosphorylation of c-Jun and N-terminal kinase (JNK), p53 and caspase cleavage the increase of-3 protein. By using FBG and 20 ginsenosides (S) together with-Rg3, the percentage of cisplatin induced apoptosis in LLC-PK1 cells leaded to increased significantly. Conclusion:FBG and its major ginsenoside 20(S)-Rg3, ameliorated cisplatin-induced nephrotoxicity in LLC-PK1 cells by blocking the JNKep-53-ecaspase-3 signaling cascade.
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