Wang Lili, Tian Xuan
The Second Department of Neurology, Cangzhou City People's Hospital, Cangzhou, China.
Planta Med. 2018 Jan;84(1):34-41. doi: 10.1055/s-0043-114865. Epub 2017 Jun 30.
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-, and interleukin-1 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.
高同型半胱氨酸水平与许多神经血管和神经退行性疾病有关。表没食子儿茶素没食子酸酯(EGCG)是绿茶多酚之一,具有潜在的抗氧化和抗炎活性。然而,EGCG是否对同型半胱氨酸诱导的神经炎症和神经退行性变有影响尚未得到研究。在本研究中,我们通过尾静脉注射同型半胱氨酸2周后,研究了EGCG对高同型半胱氨酸血症大鼠记忆缺陷、氧化应激、神经炎症和神经退行性变的影响。我们发现补充EGCG可以挽救同型半胱氨酸诱导的空间记忆缺陷。EGCG治疗显著降低了同型半胱氨酸处理组中丙二醛、胶质纤维酸性蛋白、肿瘤坏死因子-α和白细胞介素-1的表达,并提高了谷胱甘肽水平。在TdT介导的dUTP缺口末端标记(TUNEL)试验和荧光金B染色中,补充EGCG可以减轻凋亡神经元和神经退行性变。有趣的是,EGCG显著改善了同型半胱氨酸诱导的脑血管损伤。我们的数据表明,EGCG可能是阻止同型半胱氨酸诱导的大脑神经退行性变和神经炎症的有前途的候选药物。