Inhibition of Matrix Metalloproteinase-1 Induced by Oxidative Stress in Human Keratinocytes by Mangiferin Isolated from Anemarrhena asphodeloides

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  • CHAE Sungwook
    Aging Research Center, Korea Institute of Oriental Medicine
  • PIAO Mei Jing
    School of Medicine and Applied Radiological Science Research Institute, Jeju National University
  • KANG Kyoung Ah
    School of Medicine and Applied Radiological Science Research Institute, Jeju National University
  • ZHANG Rui
    School of Medicine and Applied Radiological Science Research Institute, Jeju National University
  • KIM Ki Cheon
    School of Medicine and Applied Radiological Science Research Institute, Jeju National University
  • YOUN Ui Joung
    Natural Products Chemistry Laboratory, College of Pharmacy, Ewha Women’s University
  • NAM Kung-Woo
    SCH-BioPharm Human Resources Development Center, Soon Chun Hyang University
  • LEE Jun Hwa
    Samsung Changwon Hospital, Sungkyunkwan University School of Medicine
  • HYUN Jin Won
    School of Medicine and Applied Radiological Science Research Institute, Jeju National University

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  • Inhibition of Matrix Metalloproteinase-1 Induced by Oxidative Stress in Human Keratinocytes by Mangiferin Isolated from<i>Anemarrhena asphodeloides</i>

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Oxidative stress is related to the synthesis of matrix metalloproteinases (MMPs), which cause skin aging. The protective effects of mangiferin derived from Anemarrhena asphodeloides were investigated against hydrogen peroxide (H2O2)-induced damage using human skin keratinocyte (HaCaT) cells. Mangiferin was found to scavenge intracellular reactive oxygen species (ROS), superoxide radicals, and hydroxyl radicals. ROS regulate MMPs gene expression and activation of proenzymes. Mangiferin inhibited H2O2-induced MMP-1 gene expression and protein levels as well as its activity. Moreover, it abrogated mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) pathway and stress-activated protein kinase/extracellular signal-regulated kinase (SEK)-c-JUN N-terminal kinase (JNK) pathway, which are induced by H2O2 treatment. And, it inhibited DNA binding activity of activator protein-1 (AP-1), a transcription factor of MMP-1 and downstream of ERK and JNK. Finally, it protected the human skin keratinocytes from H2O2-induced cell death. Taken together, these results indicate that mangiferin attenuated H2O2-induced MMP-1 activation via inhibition of ERK and JNK pathway and AP-1.

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