ArticleExperimental and therapeutic medicine2017
Echinocystic acid ameliorates hyperhomocysteinemia-induced vascular endothelial cell injury through regulating NF-κB and CYP1A1.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Role and Relationship Between Homocysteine and HMolecular neurobiology · 2025Review
- Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025Review
- Identification of Fatty Acid Metabolism Disorder-Related Gene Signature in Septic Cardiomyopathy.Journal of inflammation research · 2025Article
- Nonlinear Relationship Between Homocysteine and Mild Cognitive Impairment in Early Parkinson's Disease: A Cross-Sectional Study.Neuropsychiatric disease and treatment · 2024Article
- Relationship Among Homocysteine, Inflammation and Cognitive Impairment in Patients with Acute Ischemic Stroke and Transient Ischemic Attack.Neuropsychiatric disease and treatment · 2021Article
- Echinocystic acid provides a neuroprotective effect via the PI3K/AKT pathway in intracerebral haemorrhage mice.Annals of translational medicine · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study investigated the role of echinocystic acid (EA) on the expression of nuclear factor (NF)-κB and cytochrome P450 1A1 (CYP1A1), and aortic morphology, in a rat model of hyperhomocysteinemia (Hhcy). A total of 50 Sprague Dawley rats were randomly divided into five groups as follows: Normal control (NC), model control (MC), vitamin control (VC; folic acid 1 mg/kg + vitamin B2 2 mg/kg + vitamin B12 10u g/kg), EA1 (20 mg/kg EA) and EA2 (40 mg/kg EA). Plasma homocysteine (Hcy) levels were determined via high performance liquid chromatography, and the morphology of the aorta was investigated using hematoxylin and eosin staining. Furthermore, aortic mRNA and protein levels of NF-κB and CYP1A1 were measured using reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. Plasma Hcy levels, and aortic mRNA and protein levels of NF-κB and CYP1A1, were significantly lower in the EA-treated group compared with the MC group (all P<0.05). However, the aortic morphology remained normal, including the endothelial cells of the inner layer, and smooth muscle cells of the media layer and adventitia. In conclusion, the results of the present study indicate that EA has a protective role on vascular endothelial cells in Hhcy through decreasing plasma Hcy, and thus NF-κB and CYP1A1 expression.
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