Planta Med 2018; 84(01): 34-41
DOI: 10.1055/s-0043-114865
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Epigallocatechin-3-Gallate Protects against Homocysteine-Induced Brain Damage in Rats

Lili Wang
The Second Department of Neurology, Cangzhou City Peopleʼs Hospital, Cangzhou, China
Xuan Tian
The Second Department of Neurology, Cangzhou City Peopleʼs Hospital, Cangzhou, China
› Author Affiliations
Further Information

Publication History

received 28 March 2017
revised 08 June 2017

accepted 18 June 2017

Publication Date:
30 June 2017 (eFirst)


High levels of homocysteine are implicated in many neurovascular and neurodegeneration diseases. Epigallocatechin 3-gallate (EGCG), one of green tea polyphenols, has potential anti-oxidative and anti-inflammatory activities. However, it has not been explored whether EGCG has an effect on homocysteine-induced neuro-inflammation and neurodegeneration. In this study, we investigated the effects of EGCG on memory deficit, oxidative stress, neuro-inflammation, and neurodegeneration in hyper-homocysteinemic rats after a 2 wk homocysteine injection by vena caudalis. We found that supplementation of EGCG could rescue deficit of spatial memory induced by homocysteine. Treatment of EGCG significantly reduced the expression of malondialdehyde, glial fibrillary acidic protein, tumor necrosis factor-α, and interleukin-1β and increased glutathione level in the homocysteine-treated group. In TdT-mediated dUTP nick end labeling (TUNEL) assay and Fluoro-Jade B staining, supplementation of EGCG could attenuate the apoptotic neurons and neurodegeneration. Interestingly, EGCG significantly ameliorated homocysteine-induced cerebrovascular injury. Our data suggest that EGCG could be a promising candidate for arresting homocysteine-induced neurodegeneration and neuro-inflammation in the brain.