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Methyl 3,4‐dihydroxybenzoate protects primary cortical neurons against Aβ 25–35 ‐induced neurotoxicity through mitochondria pathway
Author(s) -
Zhou XiaoWen,
Zhang Zheng,
Su ChaoFen,
Lv RuoHua,
Zhou Xing,
Cai Liang,
Wang ChenYu,
Yan Li,
Zhang Wei,
Luo HuanMin
Publication year - 2013
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23235
Subject(s) - neurotoxicity , neuroprotection , apoptosis , reactive oxygen species , chemistry , mitochondrion , cortical neurons , viability assay , microbiology and biotechnology , neurotrophic factors , pharmacology , biochemistry , biology , toxicity , receptor , organic chemistry
Amyloid‐β peptides (Aβ), which can aggregate into oligomers or fibrils in neurons, play a critical role in the pathogenesis of Alzheimer's disease (AD). Methyl 3,4‐dihydroxybenzoate (MDHB), a phenolic acid compound, has been reported to have antioxidative and neurotrophic effects. The present study investigated the neuroprotective effects of MDHB against Aβ‐induced apoptosis in rat primary cortical neutons. The primary cortical neurons were pretreated with different concentrations of MDHB for 24 hr, then incubated with 10 μM Aβ 25–35 for 24 hr. The results showed that Aβ 25–35 could induce neurotoxicity as evidenced by the decreased cell viability and the increased apoptotic rate. In parallel, Aβ 25–35 significantly increased the reactive oxygen species accumulation and decreased mitochondrial membrane potential. However, pretreatment of the primary cortical neurons with MDHB could effectively suppress these cellular events caused by Aβ 25–35 exposure. In addition, MDHB could increase the level of Bcl‐2, decrease the level of Bax, and inhibit the activation of caspase‐9 and caspase‐3 in Aβ 25–35 ‐treated primary cortical neurons. All these results were beneficial in their protective effect against Aβ‐induced neurotoxicity. Our results suggest that MDHB has a neuroprotective effect that provides a pharmacological basis for its clinical use in the treatment of AD. © 2013 Wiley Periodicals, Inc.