(−)-Epigallocatechin Gallate Inhibits Asymmetric Dimethylarginine-Induced Injury in Human Brain Microvascular Endothelial Cells

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.

RP105 ameliorates hypoxia̸reoxygenation injury in cardiac microvascular endothelial cells by suppressing TLR4̸MAPKs̸NF-κB signaling

“…However, the exact mechanisms that sensitize CMECs to H̸R injury remain incompletely understood and the endogenous mechanisms that may regulate the disassociation between TLR4 and CMEC H̸R injury are not known. Previous studies revealed that the activity of p-ERK1̸2 was involved in the inflammatory injury of brain microvascular endothelial cells caused by mock ischemic treatment (31), and its participation in inducing apoptosis under hypoxic conditions was also verified (32,33). Moreover, the pro-inflammatory and -apoptotic patterns of p-p38 MAPK and p-JNK activation in the ischemic endothelium have also been extensively investigated (10)(11)(12)(13)(14)(15)27,34).…”

“…and̸or MAPKs inhibition (10,(12)(13)(14)(15)27,33). However, whether MAPKs and NF-κB participate in the multifarious pathogenesis of CMEC H̸R injury via TLR4-mediated mechanisms has not been fully elucidated.…”

Suppressing glucose metabolism with epigallocatechin-3-gallate (EGCG) reduces breast cancer cell growth in preclinical models

“…In agreement, EGCG has been shown to directly target both tumor cells and tumor vasculature, thereby inhibiting tumor growth, and angiogenesis of breast cancer, by the inhibition of HIF-1α and as well as VEGF expression. 63 Moreover, because EGCG has been shown to also protect endothelial cells through various mechanisms, [64][65][66] we cannot rule out that the inhibitory effect of EGCG on VEGF is, in part, the result of its effect on endothelial cells.…”

Asymmetric dimethylarginine downregulates sarco/endoplasmic reticulum calcium-ATPase 3 and induces endoplasmic reticulum stress in human umbilical vein endothelial cells

“…There is evidence of a strong association among atherosclerosis risk factors and ADMA levels ( 2 – 6 ). In previous reports, ADMA induced endothelial cell apoptosis ( 7 , 8 ), but the molecular biological mechanisms are not clear, yet. Endothelial cell injury and apoptosis can increase vascular permeability and enhance platelet activation and aggregation, thus promoting atherosclerosis and CVD.…”