Mimosa pudica leaf extract shows protective effects in rat endometrial hyperplasia and cancer cell models

The work, led by Chandran Manimegalai Swathi and colleagues with Balamuthu Kadalmani, was published on 23 October 2026.

The researchers first characterized the phytochemical composition of the leaf extract using qualitative and quantitative analyses, measured its antioxidant efficacy, and identified its constituents by gas chromatography–mass spectrometry. They then tested antiproliferative activity against two endometrial cancer cell lines, Ishikawa and AN3CA, using MTT assays, fluorescent staining, and measurement of mRNA levels of apoptosis-related genes. These in vitro experiments assessed whether the extract could slow the growth of malignant endometrial cells and push them toward apoptotic cell death at the transcript level.

For the in vivo component, 25 female rats were divided into five groups. One group served as a control, while the remaining four received diethylstilbestrol (DES) to induce endometrial hyperplasia. Three of the hyperplasia groups were then treated with increasing doses of the M. pudica leaf extract so the team could evaluate restorative effects on the estrous cycle, ovarian structure, and uterine weight.

The researchers quantified hormones, reactive oxygen species, and mRNA expression of genes associated with inflammation (IL-6, NCOR1, and DLK1), angiogenesis (VEGF), and progression of endometrial hyperplasia (ARID1A, SMARCA4, PIK3CA, and KRAS). This gene panel was chosen to capture the molecular pathways that drive abnormal endometrial growth, new blood vessel formation, and inflammatory signaling in the uterus.

According to the results, administration of the extract restored the estrous cycle and brought the structure and function of the ovary and uterus back toward normal. The treatment also appeared to rebalance hormones and reduce inflammation in the treated animals.

In the cancer cell experiments, the extract showed antiproliferative efficacy against both Ishikawa and AN3CA cells, with the authors concluding that the extract is potentially effective against endometrial hyperplasia and the proliferation of its malignant cell lines by restoring most of the observed dysregulations up to the mRNA expression level. The authors frame this dual in vivo–in vitro design as a way to connect whole-organism outcomes with molecular mechanisms.

The findings should be interpreted with appropriate caution. The animal work involved a small number of rats and a chemically induced hyperplasia model, which may not fully recapitulate naturally occurring human disease. The in vitro results rely on two cell lines and transcript-level readouts, and the authors’ conclusions rest on mRNA expression changes rather than demonstrated clinical outcomes. No human trials were part of this study, so the therapeutic potential described remains preclinical.

By reporting coordinated changes across hormonal, inflammatory, angiogenic, and hyperplasia-associated gene pathways in a single experimental system, the work provides a transcript-level map of how M. pudica leaf extract behaved in these models.

Subject of Research: Therapeutic potential of Mimosa pudica leaf extract against endometrial hyperplasia and endometrial cancer cell proliferation in animal and in vitro models

Article Title: Mimosa pudica L. extract attenuates endometrial hyperplasia and proliferation of its malignant cell lines: transcript-level insights from a dual in vivo–in vitro model

Article References: Swathi, C. M., Vignesh, K., Archana Devi, C., & Kadalmani, B. (2026). Mimosa pudica L. extract attenuates endometrial hyperplasia and proliferation of its malignant cell lines: transcript-level insights from a dual in vivo–in vitro model. Molecular Biology Reports, 53(1), Article 1798. https://doi.org/10.1007/s11033-026-12910-8

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12910-8

Keywords: Mimosa pudica, endometrial hyperplasia, endometrial cancer, Ishikawa cells, AN3CA cells, DES-induced hyperplasia, phytochemistry, apoptosis, gene expression, VEGF, ARID1A, SMARCA4