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
Autor: | Yu-Ling Liu, Peishuang Li, Zhen Liu, Zhen Jiang, Ruining Liang, Ling Xu, Yang Zou, Jiahua Peng, Xue-Yan Sun, Pei Fan |
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Jazyk: | angličtina |
Rok vydání: | 2017 |
Předmět: |
MAPK/ERK pathway
medicine.medical_specialty Modern medicine 030219 obstetrics & reproductive medicine Stromal cell Article Subject Cell growth business.industry p38 mitogen-activated protein kinases Cell migration lcsh:Other systems of medicine lcsh:RZ201-999 03 medical and health sciences 0302 clinical medicine Endocrinology Complementary and alternative medicine Apoptosis 030220 oncology & carcinogenesis Internal medicine Cancer research medicine Signal transduction business Research Article |
Zdroj: | Evidence-Based Complementary and Alternative Medicine, Vol 2017 (2017) Evidence-based Complementary and Alternative Medicine : eCAM |
ISSN: | 1741-4288 |
Popis: | 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. |
Databáze: | OpenAIRE |
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