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Effect of epigallocatechin‐3‐gallate on the status of DNA methylation of E‐cadherin promoter region on endometriosis mouse
Author(s) -
Guan QiHui,
Shi WenJing,
Zhou LongShu,
Tao AiLin,
Li Lu
Publication year - 2020
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.14358
Subject(s) - dna methylation , lesion , gallate , methylation , medicine , cadherin , microbiology and biotechnology , apoptosis , dna , cancer research , cell , biology , gene , pathology , gene expression , pharmacology , biochemistry
Aim To evaluate whether epigallocatechin‐3‐gallate acts on endometriosis mouse, and changes the status of DNA methylation of E‐cadherin promoter region. Methods According to our previous research, the tracing nude mouse model of endometriosis was built up and randomly divided into three groups: control group (group A), epigallocatechin‐3‐gallate group (group B) and decitabine group (group C). Normal saline, epigallocatechin‐3‐gallate and decitabine were isometrically intraperitoneally injected into each group once in 2 days. In this period, the growth situations of lesions were monitored by living image system. After 16 days, the lesions were taken out and the distribution of E‐cadherin and its methylated situation of promoter region were analyzed. Results The region of interest of ectopic lesion increased from 4th to 16th day in group A ( P < 0.01); in group B and C, the region of interest of ectopic lesion increased in the 0–8th day ( P < 0.01), and decreased in the 8–16th day ( P < 0.01). The positive expression rate of E‐cadherin in group C was higher than group B, and group B was higher than group A ( P < 0.01). The DNA methylation status of E‐cadherin promoter region in group A was higher than group B, and group B was higher than group C ( P < 0.01). Conclusion Epigallocatechin‐3‐gallate may inhibit the growth of endometrial lesion, affect the expression of E‐cadherin on the cell membrane and reduce the status of DNA methylation of E‐cadherin promoter region.