Li Qian, Cui Jing, Fang Chen, Liu Min, Min Guowen, Li Liang
J Alzheimers Dis. 2017;58(2):549-558. doi: 10.3233/JAD-170177.
Oxidative stress and neuroinflammation are mainly involved in the pathogenic mechanisms of Alzheimer's disease (AD). Amyloid-β (Aβ), the main component of senile plaques, is a kind of strong inducer of oxidative stress. Glutathione is an endogenous antioxidant protecting cells from oxidative injury. S-adenosylmethionine (SAM) produced in the methionine cycle is the primary methyl donor and the precursor of glutathione. In this study, the Aβ intrahippocampal injection rat model and cultured SH-SY5Y cells were used to explore the neuroprotective effect of SAM. We found that SAM could protect cells against Aβ-induced cellular injury by inhibition of oxidative stress and neuroinflammation. SAM administration could increase the endogenous antioxidant glutathione and potentiate the antioxidant enzymes activities. SAM might act as an antioxidant and be a potential candidate therapy for AD patients.
氧化应激和神经炎症主要参与阿尔茨海默病（AD）的发病机制。淀粉样β蛋白（Aβ）是老年斑的主要成分，是一种强大的氧化应激诱导剂。谷胱甘肽是一种内源性抗氧化剂，可保护细胞免受氧化损伤。蛋氨酸循环中产生的S-腺苷甲硫氨酸（SAM）是主要的甲基供体和谷胱甘肽的前体。在本研究中，采用海马内注射Aβ的大鼠模型和培养的SH-SY5Y细胞来探讨SAM的神经保护作用。我们发现，SAM可通过抑制氧化应激和神经炎症来保护细胞免受Aβ诱导的细胞损伤。给予SAM可增加内源性抗氧化剂谷胱甘肽并增强抗氧化酶活性。SAM可能作为一种抗氧化剂，是AD患者潜在的候选治疗药物。
