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Anti-inflammatory Effect of Flower Bud and Fruit of Sweet Persimmon, Diospyros kaki T.

  • Park, Yeo Ok (Department of Biohealth Sciences, College of Natural Sciences, Changwon National University) ;
  • Lee, Jeong Ah (Department of Biohealth Sciences, College of Natural Sciences, Changwon National University) ;
  • Park, Seong Moon (Department of Biohealth Sciences, College of Natural Sciences, Changwon National University) ;
  • Ha, Min Hee (Department of Biohealth Sciences, College of Natural Sciences, Changwon National University) ;
  • Joo, Woo Hong (Department of Biology and Chemistry, College of Natural Sciences, Changwon National University) ;
  • Kim, Dong Wan (Department of Biohealth Sciences, College of Natural Sciences, Changwon National University)
  • Received : 2020.06.04
  • Accepted : 2020.06.27
  • Published : 2020.06.30

Abstract

Various beneficial effects of sweet persimmon (Diospyros kaki T.) including anti-oxidation, anti-bacteria and viruses, anti-allergy were widely reported previously. However, the anti-inflammatory effect and its molecular mechanisms are not clear. In this study, the anti-inflammatory effect of the extracts of flower bud and fruit of sweet persimmon was investigated in LPS-treated RAW264.7 cells. Both extracts of flower bud and fruit showed strong inhibitory effect on the LPS-induced NF-κB activation. IκBα, the inhibitor of NF-κB, was increased and the expressions of NF-κB target genes, COX-2 and iNOS, were suppressed by the treatment with the extracts of flower bud and fruit. The expressions of pro-inflammatory cytokines, IL-1β, IL-6, TNF-α were also suppressed by the extracts. In addition, the LPS-induced wnt/β-catenin pathway and its related gene expressions including cyclin D1, wnt 3a, wnt 5a were suppressed by the extracts. The extracts also showed anti-oxidant activity and suppressive effect on the LPS-induced apoptosis of RAW264.7 cells. These results suggest that the flower bud and fruit of sweet persimmon display strong anti-inflammatory effect through inhibiting the pro-inflammatory signaling pathways in the cells.

Keywords

References

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