Myrrh ameliorates endometriosis by enhancing ER stress‑related apoptotic cell death

This study evaluated whether myrrh (Commiphora-derived resin) can inhibit endometriosis by combining network pharmacology with in vitro and in vivo experiments. In ovariectomized, β-estradiol–supported C57BL/6 mice with surgically induced endometriosis, oral myrrh reduced the weight of endometriotic foci at low doses, and in endometrial cell models it showed higher toxicity in 12Z cells than in T-HESCs while shifting the Bcl-2/Bax ratio to induce mitochondrial-associated apoptosis. RNA sequencing and bioinformatic analyses identified upregulation of unfolded protein response/endoplasmic reticulum stress–related pathways, and co-treatment with tauroursodeoxycholic acid (an ER stress inhibitor) abolished myrrh-induced cytotoxicity, with key UPR genes validated by RT-qPCR; a limitation is that the mechanistic work relies on ER stress inhibition in this specific experimental framework. This paper is centrally about endometriosis — it tests myrrh as an antiendometriotic agent and links its effects to ER stress–related apoptotic cell death.

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