Ping‐Chong‐Jiang‐Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway

Ruining Liang, Pei-Shuang Li, Peishuang Li, Yang Zou, Yuling Liu, Yu-Ling Liu, Zhen Jiang, Zhen Liu, Pei Fan, Ling Xu, Jia-Hua Peng, Jiahua Peng, Xueyan Sun, Xue-Yan Sun
Evidence-based complementary and alternative medicine : eCAM · 2017 · vol. 2017(1) , pp. 6489427 · doi:10.1155/2017/6489427 · PMID:28656053 · W2620777826
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Ping-Chong-Jiang-Ni formula suppressed proliferation, migration, and invasion, and induced apoptosis in ectopic endometrial stromal cells, with suppressed proliferation and increased apoptosis mediated by JNK signaling.

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Abstract

Endometriosis is a common gynecological condition in childbearing age women and its therapy in modern medicine achieves usually temporary cure. Ping-Chong-Jiang-Ni formula (PCJNF), a Chinese herbal medicine (CHM), was shown to be clinically effective on endometriosis. Meanwhile, c-Jun N-terminal kinase (JNK) signaling pathway was involved in the therapeutic process of CHM on endometriosis. Here, we explored the effect of PCJNF on the ectopic endometrial stromal cells (EESCs) from endometriosis and test whether JNK signaling was involved. After being treated with PCJNF-containing serum obtained from Sprague Dawley rat, cell proliferation, migration, invasion, and apoptosis were evaluated in EESCs, and the total and phosphorylated JNK, ERK, and p38 proteins were detected. Our results showed that PCJNF could suppress cell proliferation, migration, and invasion and induce apoptosis in EESCs. The suppressed proliferation and increased apoptosis were dependent on JNK activation. Additionally, PCJNF caused cell cycle arrest at G2/M phase and this effect was mediated by JNK signaling, while the decreased cell migration and invasion treated by PCJNF were independent of JNK signaling. In summary, our results provided the first evidence that PCJNF could suppress cell proliferation, migration, and invasion, while increasing apoptosis in EESCs, and the suppressed proliferation and enhanced apoptosis were mediated by JNK signaling.

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endometriosis

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