Hemp stem extract countered BPA estrogen signaling in cells

Cannabis sativa L. stem ethanol extract suppresses ERα-mediated endocrine disrupting effects induced by bisphenol A in a breast cancer cell line.

Ecotoxicology and environmental safety • • Highly Relevant
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AI Summary

This in vitro study asked whether an ethanol extract from Cannabis sativa stems could counteract the estrogen-receptor activity caused by bisphenol A (BPA). Researchers tested the extract in the human ERα-responsive VM7Luc4E2 breast cancer cell line, examining both ERα activation and cell proliferation. The abstract reports that the stem extract inhibited BPA-induced ERα transcriptional activation and suppressed cell proliferation.

The researchers also tested several compounds found in the extract. Cyclopentane-1,2-dione (CPD), 4-vinylguaiacol (4-VG), and 4-HMP each showed antagonistic activity against ERα activation and reduced proliferation in the cell model. The reported mechanisms differed: CPD blocked estrogen-induced ERα activation without significantly changing its movement into the nucleus, while 4-VG and 4-HMP appeared to act by reducing that nuclear translocation. The extract and compounds also reduced p38 phosphorylation in the MAPK signaling pathway. Because this was a laboratory cell study with no human participants or clinical outcomes, it cannot establish that hemp stems prevent endocrine disruption or provide a health benefit in people; this is an abstract-based summary, not a full-text review.

💡 Key Findings

1
In a human breast cancer cell model, Cannabis sativa stem ethanol extract inhibited BPA-induced ERα activation and suppressed cell proliferation.
High
80%
2
The stem compounds cyclopentane-1,2-dione, 4-vinylguaiacol, and 4-HMP each showed antagonistic effects on ERα activation and cell proliferation in the cell model.
Good
75%
3
The compounds appeared to act through different mechanisms: CPD inhibited estrogen-induced ERα activation without significantly affecting nuclear translocation, whereas 4-VG and 4-HMP suppressed that translocation.
Good
70%
4
The reported suppression of cell proliferation was associated with downregulation of p38 phosphorylation in the MAPK pathway.
Good
65%

📄 Original Abstract

Cannabis sativa L. (hemp), a Cannabaceae family member, has been extensively studied for its diverse secondary metabolites with physiological activities. However, stems that lack detectable levels of the delta-9-tetrahydrocannabinol have been understudied. Herein, we aimed to investigate the antagonistic effects using C. sativa L. stem ethanol extract (CSE) and its bioactive compounds on human ERα activity induced by exogenous estrogen, bisphenol A (BPA), through genomic and non-genomic pathways. CSE inhibited BPA-induced ERα transcriptional activation in VM7Luc4E2 cells and suppressed cell proliferation. Among the secondary metabolites in CSE, cyclopentane-1,2-dione (CPD), 4-vinylguaiacol (4-VG), and 4-([1E]-hydroxy-1-propenyl)-2-methoxyphenol (4-HMP) exhibited antagonistic effects on ERα transcriptional activation and inhibited cell proliferation. Cell proliferation suppression was mediated by downregulation of p38 phosphorylation in the MAPK signaling pathway. CPD inhibited exogenous estrogen-induced activation of ERα without significant affecting the translocation of cytosolic ERα to the nucleus. In contrast, 4-VG and 4-HMP exerted antagonistic effect based on suppressing the nuclear translocation of cytosolic ERα. Collectively, the results showed that CSE suppressed ERα-mediated endocrine disruption induced by exogenous estrogen, suggesting its potential as a natural ingredient to reduce endocrine disruption from dietary sources.

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