Affiliations: Department of Pathology, School of Basic Medical Sciences, Capital Medical University, Beijing, China
Correspondence:
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Correspondence to: Liang Li, Department of Pathology, School of Basic Medical Sciences, Capital Medical University, 10 Xi Tou Tiao, You An Men street, Beijing 100069, China. Tel.: +86 010 83911698; Fax: +86 010 83911699; E-mail: [email protected].
Abstract: 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.
