Chrysin leads to cell death in endometriosis by regulation of endoplasmic reticulum stress and cytosolic calcium level

Soomin Ryu, Fuller W. Bazer, Whasun Lim, Gwonhwa Song

    Research output: Contribution to journalArticlepeer-review

    17 Citations (Scopus)

    Abstract

    Chrysin is a natural compound derived from honey, propolis, or passion flowers and has many functional roles, such as antiinflammatory and antiangiogenesis effects. Although endometriosis is a benign gynecological disease, there is a need to identify the pathology and develop a therapy for endometriosis. Elucidating the biological mechanism of chrysin on endometriosis will improve the understanding of endometriosis. In this study, we confirmed the apoptotic effects of chrysin in human endometriotic cells using End1/E6E7 (endocervix-derived endometriotic cells) and VK2/E6E7 (vaginal mucosa-derived epithelial endometriotic cells). The results showed that chrysin suppressed the proliferation of endometriosis and induced programmed cell death through changing the cell cycle proportion and increasing the cytosolic calcium level and generation of reactive oxygen species. In addition, chrysin activated endoplasmic reticulum (ER) stress by stimulating the unfolded protein response proteins, especially the 78-kDa glucose-regulated protein–PRKR-like ER kinase (PERK)–eukaryotic translation initiation factor 2α (eIF2α) pathway in both endometriotic cell lines. Furthermore, chrysin inactivated the intracellular phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB, also known as AKT) signaling pathway in a dose-dependent manner. Collectively, the results of this study indicated that chrysin induced programmed cell death by activating the ER stress response and inactivating the PI3K signaling pathways in human endometriotic cells.

    Original languageEnglish
    Pages (from-to)2480-2490
    Number of pages11
    JournalJournal of Cellular Physiology
    Volume234
    Issue number3
    DOIs
    Publication statusPublished - 2019 Mar

    Bibliographical note

    Funding Information:
    The study was supported by the Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health & Welfare, Republic of Korea with the contract grant numbers HI17C0929 and HI15C0810.

    Funding Information:
    The Korea Health Technology R&D Project through the Korea Health Industry Development Institute funded by the Ministry of Health & Welfare, Republic of Korea, Grant/Award Numbers: HI17C0929, HI15C0810

    Publisher Copyright:
    © 2018 Wiley Periodicals, Inc.

    Keywords

    • apoptosis
    • chrysin
    • endometriosis
    • endoplasmic reticulum stress
    • phosphoinositide 3-kinase/AKT signal pathway

    ASJC Scopus subject areas

    • Physiology
    • Clinical Biochemistry
    • Cell Biology

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