Effect of genistein on proinflammatory cytokines and estrogen receptor–β in mice model of endometriosis

Sutrisno Sutrisno, Rr. Catur Leny Wulandari, Dwi Wahyu Wulan Sulistyowati, Ratna Feti Wulandari, Endang Sri Wahyuni, Yuyun Yueniwati, Sanarto Santoso
In: Asian Pacific Journal of Reproduction · 2015 · vol. 4(2) , pp. 96–99 · doi:10.1016/s2305-0500(15)30003-8 · W2520467978
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Genistein treatment in a mouse endometriosis model reduced proinflammatory cytokines, NF-κB activation, and estrogen receptor-β expression.

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Abstract

To investigate the effect of genistein on proinflammatory cytokines, NF-κ B activation, and estrogen receptor-β expression in a mice model of endometriosis. Forty female mice (Mus musculus) were divided into eight groups (n=5 each), including the control (untreated) group, endometriosis group, and the endometriosis groups were given various doses of genistein (at doses of 50; 100; 200; 300; 400; 500 mg/day). Analysis of TNF-α, IL-1β, IL-6, and IL-8 level were done by ELISA technically. Analysis of estrogen receptor-β and NF-κB were done by immunohistochemistry. The level of TNF-α, IL-1β, IL-6, and IL-8 were significantly higher in the EM group compared to the untreated control group (P<0.05). All doses genistein significantly prevented EM-induced increase in TNF-α level (P0.05). These increased levels of IL-1β, IL-6, adn IL-8 in the EM group were significantly reduced by all doses of genistein. There were significantly (P<0.05) increased estrogen receptor-β expression and NF-κB activation in EM group compared to untreated group. Only first and fourth dose significantly (P0.05). All doses genistein significantly prevented EM-induced increase in NF-κB activation (P<0.05), to reach the expression on control group. In conclusion, genistein prohibits the increase in proinflammatory cytokines, NF-κB, and estrogen receptor-β expression in a mice model of endometriosis.

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endometriosis

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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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