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Beneficial effects of fermented black ginseng and its ginsenoside 20(S)-Rg3 against cisplatin-induced nephrotoxicity in LLC-PK1 cells

  • Han, Myoung-Sik (Department of Surgery, University of Ulsan College of Medicine) ;
  • Han, Im-Ho (Department of Chemistry, Gangneung-Wonju National University) ;
  • Lee, Dahae (College of Korean Medicine, Gachon University) ;
  • An, Jun Min (GINSENG BY PHARM Co., Ltd.) ;
  • Kim, Su-Nam (Natural Products Research Institute, Korea Institute of Science and Technology) ;
  • Shin, Myoung-Sook (Natural Products Research Institute, Korea Institute of Science and Technology) ;
  • Yamabe, Noriko (College of Korean Medicine, Gachon University) ;
  • Hwang, Gwi Seo (College of Korean Medicine, Gachon University) ;
  • Yoo, Hye Hyun (College of Pharmacy, Hanyang University) ;
  • Choi, Suk-Jung (Department of Chemistry, Gangneung-Wonju National University) ;
  • Kang, Ki Sung (College of Korean Medicine, Gachon University) ;
  • Jang, Hyuk-Jai (Department of Surgery, University of Ulsan College of Medicine)
  • Received : 2015.05.27
  • Accepted : 2015.06.25
  • Published : 2016.04.15

Abstract

Background: Nephrotoxicity is a common side effect of medications. Panax ginseng is one of the best-known herbal medicines, and its individual constituents enhance renal function. Identification of its efficacy and mechanisms of action against drug-induced nephrotoxicity, as well as the specific constituents mediating this effect, have recently emerged as an interesting research area focusing on the kidney protective efficacy of P. ginseng. Methods: The present study investigated the kidney protective effect of fermented black ginseng (FBG) and its active component ginsenoside 20(S)-Rg3 against cisplatin (chemotherapy drug)-induced damage in pig kidney (LLC-PK1) cells. It focused on assessing the role of mitogen-activated protein kinases as important mechanistic elements in kidney protection. Results: The reduced cell viability induced by cisplatin was significantly recovered with FBG extract and ginsenoside 20(S)-Rg3 dose-dependently. The cisplatin-induced elevated protein levels of phosphorylated c-Jun N-terminal kinase (JNK), p53, and cleaved caspase-3 were decreased after cotreatment with FBG extract or ginsenoside 20(S)-Rg3. The elevated percentage of apoptotic LLC-PK1 cells induced by cisplatin treatment was significantly abrogated by cotreatment with FBG and the ginsenoside 20(S)-Rg3. Conclusion: FBG and its major ginsenoside 20(S)-Rg3, ameliorated cisplatin-induced nephrotoxicity in LLC-PK1 cells by blocking the JNKep53ecaspase-3 signaling cascade.

Keywords

References

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