Costunolide Induces Apoptosis in Human Endometriotic Cells through Inhibition of the Prosurvival Akt and Nuclear Factor Kappa B Signaling Pathway

Ji-Hyun Kim, Ji‐Hyun Kim, Yeong‐In Yang, Yeong-In Yang, Kyung‐Tae Lee, Kyung-Tae Lee, Hee-Juhn Park, Jung‐Hye Choi, Jung-Hye Choi
Biological & pharmaceutical bulletin · 2011 · vol. 34(4) , pp. 580–585 · doi:10.1248/bpb.34.580 · PMID:21467650 · W2096916927
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Costunolide inhibits endometriotic cell viability and induces apoptosis by suppressing the prosurvival Akt and NFκB pathways, leading to caspase activation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

The study evaluated the effects of costunolide, a sesquiterpene lactone, on proliferation and apoptosis in 11Z and 12Z human endometriotic epithelial cells compared with immortalized endometrial cells (HES). Costunolide significantly reduced cell viability, induced time-dependent apoptosis with sub-G1 accumulation, and activated caspase-3, -8, and -9 in a dose- and time-dependent manner, with z-VAD-fmk reversing the viability inhibition. Mechanistically, costunolide suppressed Akt and NFκB signaling and decreased expression of anti-apoptotic proteins Bcl-xL and XIAP in 11Z cells. This paper is centrally about endometriosis — it tests costunolide’s ability to trigger apoptosis in human endometriotic epithelial cells via inhibition of Akt/NFκB and downregulation of anti-apoptotic factors.

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Abstract

Endometriosis, a disease affecting 5-15% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Costunolide, a sesquiterpene lactone, has anti-proliferative and pro-apoptotic activities that may be efficacious in therapy for endometriosis. In the present study, we investigated the effect of costunolide on the cell growth and apoptosis of endometriotic cells. We found that costunolide significantly inhibited the cell viability of 11Z and 12Z human endometriotic epithelial cells. Interestingly, endometriotic cells were more sensitive to costunolide treatment than immortalized endometrial cells (HES). Costunolide induced apoptosis of 11Z cells in a time-dependent manner as shown by accumulation of sub-G1 population. In addition, treatment with costunolide induced the activation of caspase-3, -8, and -9 in a dose- and time-dependent manner. Pretreatment with the broad caspase inhibitor z-VAD-fmk significantly reversed the costunolide-induced inhibition of cell viability in 11Z cells. We further demonstrated that costunolide inhibited the activation of Akt and nuclear factor kappa B (NFκB) and the expression of anti-apoptotic factors B-cell lymphoma-extra lage (Bcl-xL) and X-linked inhibitor of apoptosis protein (XIAP) in 11Z cells. These results suggest that costunolide induces apoptosis in human endometriotic epithelial cells by inhibiting the prosurvival NFκB and Akt pathway, leading to the downregulation of anti-apoptotic protein Bcl-xL and XIAP and the activation of caspases.
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Note Costunolide Induces Apoptosis in Human Endometriotic Cells through Inhibition of the Prosurvival Akt and Nuclear Factor Kappa B Signaling Pathway 2011 Volume 34 Issue 4 Pages 580-585 Details Abstract Endometriosis, a disease affecting 5—15% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Costunolide, a sesquiterpene lactone, has anti-proliferative and pro-apoptotic activities that may be efficacious in therapy for endometriosis. In the present study, we investigated the effect of costunolide on the cell growth and apoptosis of endometriotic cells. We found that costunolide significantly inhibited the cell viability of 11Z and 12Z human endometriotic epithelial cells. Interestingly, endometriotic cells were more sensitive to costunolide treatment than immortalized endometrial cells (HES). Costunolide induced apoptosis of 11Z cells in a time-dependent manner as shown by accumulation of sub-G1 population. In addition, treatment with costunolide induced the activation of caspase-3, -8, and -9 in a dose- and time-dependent manner. Pretreatment with the broad caspase inhibitor z-VAD-fmk significantly reversed the costunolide-induced inhibition of cell viability in 11Z cells. We further demonstrated that costunolide inhibited the activation of Akt and nuclear factor kappa B (NFκB) and the expression of anti-apoptotic factors B-cell lymphoma-extra lage (Bcl-xL) and X-linked inhibitor of apoptosis protein (XIAP) in 11Z cells. These results suggest that costunolide induces apoptosis in human endometriotic epithelial cells by inhibiting the prosurvival NFκB and Akt pathway, leading to the downregulation of anti-apoptotic protein Bcl-xL and XIAP and the activation of caspases. © 2011 The Pharmaceutical Society of Japan Favorites & Alerts Recently viewed articles

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Apoptosis Endometriosis Endometrium NF-kappa B Plant Extracts Proto-Oncogene Proteins c-akt Sesquiterpenes Amino Acid Chloromethyl Ketones Amino Acid Chloromethyl Ketones Apoptosis Caspase Inhibitors Cell Line Cell Proliferation Cell Proliferation Dose-Response Relationship, Drug Endometriosis Endometriosis Endometrium Endometrium Enzyme Inhibitors

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