ArticleMolecular and cellular biochemistry2012
Protective effects of 7-difluoromethyl-5,4'-dimethoxygenistein against human aorta endothelial injury caused by lysophosphatidyl choline.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Metabolic alterations and potential biomarkers in unstable angina investigated by lipidomic analysis.Frontiers in molecular biosciences · 2026Article
- DFMG attenuates the activation of macrophages induced by co‑culture with LPC‑injured HUVE‑12 cells via the TLR4/MyD88/NF‑κB signaling pathway.International journal of molecular medicine · 2018Article
- DFMG reverses proliferation and migration of vascular smooth muscle cells induced by co-culture with injured vascular endothelial cells via suppression of the TLR4-mediated signaling pathway.Molecular medicine reports · 2018Article
- Plasma metabolomic profiling to reveal antipyretic mechanism of Shuang-huang-lian injection on yeast-induced pyrexia rats.PloS one · 2014Article
- Effect of 7-difluoromethyl-5, 4'-dimethoxygenistein on aorta atherosclerosis in hyperlipidemia ApoE(-/-) mice induced by a cholesterol-rich diet.Drug design, development and therapy · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
7-Difluoromethyl-5,4'-dimethoxygenistein (DFMG) is an active new derivative of genistein (GEN). It has shown effective protection in vascular endothelial injury. To further investigate its potential protective effects and its mechanism probably related to atherosclerosis, in present study, human aorta endothelial cells (HAECs) were chosen and treated with various concentrations of lysophosphatidyl choline (LPC) to establish an experimental model. Results showed that 10.0 μmol/l of LPC was optimal for inducing HAEC injury. DFMG pretreatment was able to prevent HAEC injury induced by LPC and restore cell viability in a concentration-dependent manner. The protective efficacy of DFMG (10.0 μmol/l) was significantly greater than that of GEN (10.0 μmol/l) and vitamin E (50.0 μmol/l). The mechanisms underlying the protective effects of DFMG are related to the activation of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase and to the clearance of intracellular reactive oxygen species. DFMG inhibits the apoptosis of HAECs mediated by LPC involving the blockage of the mitochondrial apoptotic pathway.
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