DOI QR코드

DOI QR Code

Protective effect of Korean Red Ginseng against FK506-induced damage in LLC-PK1 cells

  • Lee, Dahae (School of Pharmacy, Sungkyunkwan University) ;
  • Kang, Ki Sung (College of Korean Medicine, Gachon University) ;
  • Yu, Jae Sik (School of Pharmacy, Sungkyunkwan University) ;
  • Woo, Jung-Yoon (The Korea Ginseng Research Institute, Korea Ginseng Corporation) ;
  • Hwang, Gwi Seo (College of Korean Medicine, Gachon University) ;
  • Eom, Dae-Woon (Department of Pathology, University of Ulsan College of Medicine, Gangneung Asan Hospital) ;
  • Baek, Seung-Hoon (College of Pharmacy, Ajou University) ;
  • Lee, Hye Lim (College of Korean Medicine, Gachon University) ;
  • Kim, Ki Hyun (School of Pharmacy, Sungkyunkwan University) ;
  • Yamabe, Noriko (College of Korean Medicine, Gachon University)
  • 투고 : 2016.02.23
  • 심사 : 2016.05.15
  • 발행 : 2017.07.15

초록

Background: Compound FK506 is an immunosuppressant agent that is frequently used to prevent rejection of solid organs upon transplant. However, nephrotoxicity due to apoptosis and inflammatory response mediated by FK506 limit its usefulness. In this study, the protective effect of Korean Red Ginseng (KRG) against FK506-induced damage in LLC-PK1 pig kidney epithelial cells was investigated. Methods: LLC-PK1 cells were exposed to FK506 with KRG and cell viability was measured. Western blotting and RT-PCR analyses evaluated protein expression of MAPKs, caspase-3, and KIM-1. TLR-4 gene expression was assessed. Caspase-3 activities were also determined. The number of apoptotic cells was measured using an image-based cytometric assay. Results: The reduction in LLC-PK1 cell viability by $60{\mu}M$ FK506 was recovered by KRG cotreatment in a dose-dependent manner. The phosphorylation of p38, p44/42 MAPKs (ERK), KIM-1, cleaved caspase-3, and TLR-4 mRNA expression was increased markedly in LLC-PK1 cells treated with $60{\mu}M$ FK506. However, with the exception of p-ERK, elevated levels of p-p38, KIM-1, cleaved caspase-3, and TLR-4 mRNA expression were significantly decreased after cotreatment with KRG. Activity level of caspase-3 was also attenuated by KRG cotreatment. Moreover, image-based cytometric assay showed that apoptotic cell death was increased by $60{\mu}M$ FK506 treatment, whereas it was decreased after cotreatment with KRG. Conclusion: Taken together, these results suggest that the molecular mechanism of KRG in the FK506-induced nephrotoxicity may lead to the development of an adjuvant for the inhibition of adverse effect FK506 in the kidney.

키워드

참고문헌

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