Research Papers:

Ginseng Rh2 protects endometrial cells from oxygen glucose deprivation/re-oxygenation

Xiao-Fang Tang, Hai-Yan Liu, Ling Wu, Min-Hui Li, Shu-Ping Li and Hong-Bin Xu _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:105703-105713. https://doi.org/10.18632/oncotarget.22390

Metrics: PDF 1290 views  |   HTML 1941 views  |   ?  


Xiao-Fang Tang1,*, Hai-Yan Liu2,*, Ling Wu2,*, Min-Hui Li1, Shu-Ping Li1 and Hong-Bin Xu1

1Obstetrics and Gynecology Department, Changzhou Second People's Hospital, Changzhou, China

2Obstetrics and Gynecology Department, Maternal and Child Health Care Hospital of Yancheng City, Yancheng, China

*Co-first authors

Correspondence to:

Hong-Bin Xu, email: [email protected]

Shu-Ping Li, email: [email protected]

Keywords: Ginseng Rh2; oxygen glucose deprivation/re-oxygenation; endometrial cells; programmed necrosis; cyclophilin

Received: October 02, 2017    Accepted: October 27, 2017    Published: November 11, 2017


In this study, oxygen glucose deprivation/re-oxygenation (OGDR) was applied to cultured endometrial cells to mimic ischemic-reperfusion injuries. We also tested the potential effect of Ginseng Rh2 (GRh2) against the process. In established T-HESC human endometrial cells and primary murine endometrial cells, GRh2 largely inhibited OGDR-induced viability reduction and cell death. Remarkably, OGDR induced programmed necrosis in the endometrial cells, evidenced by cyclophilin D-p53-adenine nucleotide translocator 1 (ANT-1) mitochondrial association, mitochondrial depolarization, reactive oxygen species production, and lactate dehydrogenase release. Notably, such effects by OGDR were largely attenuated with co-treatment of GRh2. Further, cyclophilin D inhibition or knockdown also protected endometrial cells from OGDR. On the other hand, forced over-expression of cyclophilin D facilitated OGDR-induced T-HESC cell necrosis, which was dramatically inhibited by GRh2. Together, GRh2 protects endometrial cells from OGDR possibly via inhibiting CypD-dependent programmed necrosis pathway.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 22390