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Epicatechin and its derivate Epicatechin gallate inhibit prostatic stromal cell proliferation through selective MAPK-ERK44/42 pathway |
Hits 1731 Download times 1467 Received:November 15, 2016 |
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DOI
10.11656/j.issn.1672-1519.2017.03.15 |
Key Words
Epicatechin gallate;Epicatechin;benign prostatic hyperplasia;cell proliferation;MAPK pathway |
Author Name | Affiliation | E-mail | JIAO Chan-yuan | Tianjin Universiry of Traditional Chinese Medicine, Tianjin State Key Laboratory of Modern Chinese Medicine, Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae of Ministry of Education, Tianjin 300193, China | | JING Chun-hui | Tianjin Universiry of Traditional Chinese Medicine, Tianjin State Key Laboratory of Modern Chinese Medicine, Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae of Ministry of Education, Tianjin 300193, China | | YUAN Xiao-ting | Tianjin Universiry of Traditional Chinese Medicine, Tianjin State Key Laboratory of Modern Chinese Medicine, Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae of Ministry of Education, Tianjin 300193, China | | MIAO Lin | Tianjin Universiry of Traditional Chinese Medicine, Tianjin State Key Laboratory of Modern Chinese Medicine, Key Laboratory of Pharmacology of Traditional Chinese Medical Formulae of Ministry of Education, Tianjin 300193, China | mmmlin7180@hotmail.com |
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Abstract
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[Objective] To study the effect and mechanism of Epicatechin (EC) and its derivate Epicatechin gallate (ECG) in cynomorium songaricum on the proliferation of prostrate stromal cell line WPMY-1.[Methods] WPMY-1 cells were treated with different doses of ECG and EC in vitro. MTT assay was performed to detect the effects of ECG and EC on WPMY-1 cell proliferation. PCR and western blot were performed to detect the mRNA and protein expressions of proliferating cell nuclear antigen proliferating cell nuclear antigen(PCNA) separately in WPMY-1 cells treated with ECG or EC. The phosphorylation levels of MAPK signaling pathway ERK44/42, P38, and SAPK/JNK were then detected by western blot in WPMY-1 cells after treatment with ECG or EC. The effects of different MAPK signalings on ECG and EC-suppressed cell proliferation were investigated in WPMY-1 cells after treatment with or without ERK44/42 agonist C6-Ceramide (C6) or dual agonist Anisomycin (ANI) of P38, SAPK/JNK.[Results] Both ECG and EC (1 nmol/L to 10 μmol/L) inhibited the proliferation of WPMY-1 cells significantly (P<0.01) and PCNA expressions in mRNA and protein levels in WPMY-1 cell(P<0.05). the constitutive phosphorylation levels of ERK44/42 and SAPK/JNK were significantly suppressed by ECG and EC, which of P38 was not altered. After the adding of C6 blocked ECG and EC-induced suppression of WPMY-1 cell proliferation(P<0.05 or P<0.01). The change of cell proliferation was not significant after the adding of ANI.[Conclusion] ECG and EC inhibit prostatic stromal cell proliferation through ERK44/42 pathway, which provides evidence for their mechanism on benign prostatic hyperplasia prevention. |
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