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Epicatechin and its derivate Epicatechin gallate inhibit prostatic stromal cell proliferation through selective MAPK-ERK44/42 pathway
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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 NameAffiliationE-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 
Abstract
    [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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