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Korean Red Ginseng alleviates dehydroepiandrosterone-induced polycystic ovarian syndrome in rats via its antiinflammatory and antioxidant activities

  • Choi, Jong Hee (Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University) ;
  • Jang, Minhee (Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University) ;
  • Kim, Eun-Jeong (Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University) ;
  • Lee, Min Jung (Department of Science in Korean Medicine and Brain Korea 21 Plus Program, Graduate School, Kyung Hee University) ;
  • Park, Kyoung Sun (Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation) ;
  • Kim, Seung-Hyun (College of Veterinary Medicine, Chonnam National University) ;
  • In, Jun-Gyo (Laboratory of Analysis R&D Headquarters, Korea Ginseng Corporation) ;
  • Kwak, Yi-Seong (Korea Ginseng Research Institute, Korea Ginseng Corporation) ;
  • Park, Dae-Hun (Department of Nursing, Dongshin University) ;
  • Cho, Seung-Sik (Department of Pharmacy, College of Pharmacy and Natural Medicine Research Institute, Mokpo National University) ;
  • Nah, Seung-Yeol (Ginsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine and Bio/Molecular Informatics Center, Konkuk University) ;
  • Cho, Ik-Hyun (Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University) ;
  • Bae, Chun-Sik (College of Veterinary Medicine, Chonnam National University)
  • Received : 2018.12.04
  • Accepted : 2019.08.20
  • Published : 2020.11.15

Abstract

Background: Beneficial effects of Korean Red Ginseng (KRG) on polycystic ovarian syndrome (PCOS) remains unclear. Methods: We examined whether pretreatment (daily from 2 hours before PCOS induction) with KRG extract in water (KRGE; 75 and 150 mg/kg/day, p.o.) could exert a favorable effect in a dehydroepian-drosterone (DHEA)-induced PCOS rat model. Results: Pretreatment with KRGE significantly inhibited the elevation of body and ovary weights, the increase in number and size of ovarian cysts, and the elevation of serum testosterone and estradiol levels induced by DHEA. Pretreatment with KRGE also inhibited macrophage infiltration and enhanced mRNA expression levels of chemokines [interleukin (IL)-8, monocyte chemoattractant protein-1), proinflammatory cytokines (IL-1β, IL-6), and inducible nitric oxide synthase in ovaries induced by DHEA. It also prevented the reduction in mRNA expression of growth factors (epidermal growth factor, transforming growth factor-beta (EGF, TGF-β)) related to inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cell pathway and stimulation of the nuclear factor erythroid-derived 2-related factor 2 pathway. Interestingly, KRGE or representative ginsenosides (Rb1, Rg1, and Rg3(s)) inhibited the activity of inflammatory enzymes cyclooxygenase-2 and iNOS, cytosolic p-IκB, and nuclear p-nuclear factor kappa-light-chain-enhancer of activated B in lipopolysaccharide-induced RAW264.7 cells, whereas they increased nuclear factor erythroid-derived 2-related factor 2 nuclear translocation. Conclusion: These results provide that KRGE could prevent DHEA-induced PCOS via antiinflammatory and antioxidant activities. Thus, KRGE may be used in preventive and therapeutic strategies for PCOS-like symptoms.

Keywords

References

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