ArticleNeurochemical research2016
(-)-Epigallocatechin Gallate Inhibits Asymmetric Dimethylarginine-Induced Injury in Human Brain Microvascular Endothelial Cells.
Article in Neurochemical research, 2016. 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, 11 citations in OpenAlex.
- Asymmetric dimethylarginine induces maladaptive function of the blood-brain barrier.Frontiers in cell and developmental biology · 2024Article
- Role of Polyphenols as Antioxidant Supplementation in Ischemic Stroke.Oxidative medicine and cellular longevity · 2021Review
- Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical models.Food & function · 2018Article
- Asymmetric dimethylarginine downregulates sarco/endoplasmic reticulum calcium‑ATPase 3 and induces endoplasmic reticulum stress in human umbilical vein endothelial cells.Molecular medicine reports · 2017Article
- The construction of the multifunctional targeting ursolic acids liposomes and its apoptosis effects to C6 glioma stem cells.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
(-)-Epigallocatechin gallate (EGCG) is the main polyphenol component of green tea (leaves of the Camellia sinensis plant). EGCG has been reported to protect human brain microvascular endothelial cells (HBMECs) against injury in several models. However, the exact mechanism is still unclear. In the current study we found that EGCG protected against asymmetric dimethylarginine (ADMA)-induced HBMEC injury, and inhibited ADMA-induced reactive oxygen species production and malondialdehyde expression. At the same time, we found that pretreatment with EGCG attenuated the upregulation of Bax and the downregulation of Bcl-2, thus confirming the cellular protective properties of EGCG against ADMA-induced apoptosis. Furthermore, we found that EGCG inhibited ADMA-induced phosphorylation of ERK1/2 and p-38, whose inhibitors relieved HBMEC injury. In conclusion, EGCG can protect against ADMA-induced HBMEC injury via the ERK1/2 and p38 MAPK pathways, which are involved in the underlying mechanisms of HBMEC injury in cerebral infarction.
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Registered trials
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