Delphinidin induces antiproliferation and apoptosis of endometrial cells by regulating cytosolic calcium levels and mitochondrial membrane potential depolarization

Park S, Sung Soo Park, Sunwoo Park, Whasun Lim, Gwonhwa Song
Journal of cellular biochemistry · 2018 · vol. 120(4) , pp. 5072–5084 · doi:10.1002/jcb.27784 · PMID:30320921 · W2896853481
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Delphinidin inhibited human endometrial cell proliferation and induced apoptosis by increasing cytosolic calcium, decreasing mitochondrial membrane potential, and altering signaling molecule phosphorylation.

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Abstract

Endometriosis is a benign gynecological disease of women of reproductive ages, wherein endometrial cells grow ectopically, decreasing their quality of life due to chronic pelvic pain and severe dysmenorrhea. Although surgery and hormone therapies are gold standards for treating endometriosis, side effects are common and the recurrence rate is nearly 50%. Recent studies are exploring phytochemicals as pharmacological adjuvants for treating endometriosis. Delphinidin is an anthocyanin with anti-inflammatory, antioxidative, and anticancerous properties. In this study, delphinidin showed antiproliferative and apoptotic effects on human endometrial cells. Additionally, treatment with delphinidin decreased the mitochondrial membrane potential and increased cytosolic calcium levels in VK2/E6E7 and End1/E6E7 cells. Delphinidin decreased the phosphorylation of proliferative signaling molecules, including ERK1/2, AKT, P70S6K, and S6, while increasing the phosphorylation of P38 MAPK and P90RSK. These results imply that delphinidin is a novel therapeutic agent for treating and managing endometriosis, and has fewer side effects.

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Condition tags

endometriosischronic_pelvic_paindysmenorrhea

MeSH descriptors

Anthocyanins Apoptosis Calcium Cytosol Endometrium Membrane Potential, Mitochondrial Anthocyanins Apoptosis Calcium Cell Cycle Cell Cycle Cell Line Cell Proliferation Cell Proliferation Cytosol Cytosol Drug Synergism Endometriosis Endometriosis Endometrium

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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