Journal of Microbiology and Biotechnology

  • 제34권10호
  • /
  • Pages.1969-1980
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  • 2024
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  • 1017-7825(pISSN)
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  • 1738-8872(eISSN)
한국미생물·생명공학회 (The Korean Society for Microbiology and Biotechnology)
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Human Placenta Extract (HPH) Suppresses Inflammatory Responses in TNF-α/IFN-γ-Stimulated HaCaT Cells and a DNCB Atopic Dermatitis (AD)-Like Mouse Model

  • Jung Ok Lee (Department of Dermatology, College of Medicine, Chung-Ang University) ;
  • Youna Jang (Department of Dermatology, College of Medicine, Chung-Ang University) ;
  • A Yeon Park (Department of Dermatology, College of Medicine, Chung-Ang University) ;
  • Jung Min Lee (Department of Dermatology, College of Medicine, Chung-Ang University) ;
  • Kyeongsoo Jeong (Research and Development Center, Green Cross Wellbeing Corporation) ;
  • So-Hyun Jeon (Research and Development Center, Green Cross Wellbeing Corporation) ;
  • Hui Jin (Research and Development Center, Green Cross Wellbeing Corporation) ;
  • Minju Im (Research and Development Center, Green Cross Wellbeing Corporation) ;
  • Jae-Won Kim (Research and Development Center, Green Cross Wellbeing Corporation) ;
  • Beom Joon Kim (Department of Dermatology, College of Medicine, Chung-Ang University)
  • 투고 : 2024.06.28
  • 심사 : 2024.08.28
  • 발행 : 2024.10.28
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초록

Atopic dermatitis (AD), a chronic inflammatory disease, severely interferes with patient life. Human placenta extract (HPH; also known as human placenta hydrolysate) is a rich source of various bioactive substances and has widely been used to dampen inflammation, improve fatigue, exert anti-aging effects, and promote wound healing. However, information regarding HPH's incorporation in AD therapies is limited. Therefore, this study aimed to evaluate HPH's effective potential in treating AD using tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated human keratinocytes (HaCaT), immunized splenocytes, and a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model. In TNF-α /IFN-γ-stimulated HaCaT cells, HPH markedly reduced the production of reactive oxygen species (ROS) and restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1(SOD1), catalase, and filaggrin (FLG). HPH reduced interleukin (IL)-6; thymus- and activation-regulated chemokine (TARC); thymic stromal lymphopoietin (TSLP); and regulated upon activation, normal T cell expressed and presumably secreted (RANTES) levels and inhibited nuclear factor kappa B phosphorylation. Additionally, HPH suppressed the T helper 2 (Th2) immune response in immunized splenocytes. In the AD-like mouse model, it significantly mitigated the DNCB-induced elevation in infiltrating mast cells and macrophages, epidermal thickness, and AD symptoms. HPH also reduced TSLP levels and prevented FLG downregulation. Furthermore, it decreased the expression levels of IL-4, IL-5, IL-13, TARC, RANTES, and immunoglobulin E (IgE) in serum and AD-like skin lesion. Overall, our findings demonstrate that HPH effectively inhibits AD development and is a potentially useful therapeutic agent for AD-like skin disease.

키워드

과제정보

We are grateful to Dr. Dong-Hwan Kim for assisting with ideas and the experimental design.

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