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HB-EGF Ameliorates Oxidative Stress-Mediated Uterine Decidualization Damage

文献类型： 外文期刊

作者： Yu, Hai-Fan 1 ; Duan, Cui-Cui 2 ; Yang, Zhan-Qing 1 ; Wang, Yu-Si 1 ; Yue, Zhan-Peng 1 ; Guo, Bin 1 ;

作者机构： 1.Jilin Univ, Coll Vet Med, Changchun, Jilin, Peoples R China

2.Jilin Acad Agr Sci, Inst Agrofood Technol, Changchun, Jilin, Peoples R China

期刊名称：OXIDATIVE MEDICINE AND CELLULAR LONGEVITY （ 影响因子：6.543； 五年影响因子：7.454 ）

ISSN： 1942-0900

年卷期： 2019 年 2019 卷

页码：

收录情况： SCI

摘要： HB-EGF is essential for uterine decidualization, but its antioxidant function remains largely unclear. Here, we found that HB-EGF promoted the proliferation of stromal cells followed by the accelerated transition of the cell cycle from G1 to S phase and enhanced the expression or activity of Prl8a2, Prl3c1, and ALP which were well-established markers for uterine stromal cell differentiation during decidualization. Under oxidative stress, stromal cell differentiation was impaired, but this impairment was abrogated by rHB-EGF accompanied with the reduced levels of ROS and MDA which were regarded as the biomarkers for oxidative stress, indicating an antioxidant role of HB-EGF. Further analysis revealed that HB-EGF enhanced the activities of antioxidant enzymes SOD, CAT, and GPX, where addition of GPX inhibitor MS attenuated the induction of rHB-EGF on Prl8a2, Prl3c1, and ALP. Meanwhile, HB-EGF rescued the content of GSH and restored the ratio of GSH/GSSG after exposure to H2O2 but did not alter NOX activity. Along with a decline for mitochondrial superoxide, exogenous rHB-EGF improved the damage of oxidative stress on mtDNA copy number, ATP level, mitochondrial membrane potential, and activities of mitochondrial respiratory chain complex I and III whose blockage by ROT and AA led to a failure of rHB-EGF in protecting stromal cell differentiation against injury. Moreover, HB-EGF prevented stromal cell apoptosis by inhibiting Caspase-3 activity and Bax expression and recovering the level of Bcl-2 mRNA. Collectively, HB-EGF might ameliorate oxidative stress-mediated uterine decidualization damage.

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