ArticleOncotarget2017
Ginseng Rh2 protects endometrial cells from oxygen glucose deprivation/re-oxygenation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
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- GDC-0349 inhibits non-small cell lung cancer cell growth.Cell death & disease · 2020Article
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- Keap1-targeting microRNA-941 protects endometrial cells from oxygen and glucose deprivation-re-oxygenation via activation of Nrf2 signaling.Cell communication and signaling : CCS · 2020Article
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- SC79, a novel Akt activator, protects dopaminergic neuronal cells from MPPMolecular and cellular biochemistry · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.