Nirut SuwannaWipawan ThangniponRungtip Soi-ampornkulMahidol University2018-11-092018-11-092014-08-22Neuroscience Letters. Vol.578, (2014), 44-4918727972030439402-s2.0-84903850135https://repository.li.mahidol.ac.th/handle/20.500.14594/34886Alzheimer's disease is a major cause of dementia in the elderly that involves a β-amyloid peptide (Aβ)-induced cascade of an increase in oxidative damage and inflammation. The present study demonstrated the neuroprotective effects of diarylpropionitrile (DPN), a non-steroidal estrogen receptor β selective ligand, against 10μM Aβ1-42-induced oxidative stress and inflammation in primary rat cortical cell culture. Pre-treatment with 1-100nM DPN significantly decreased neuronal cell death by increasing cell viability through a significant attenuation in the reactive oxygen species level, downregulation of pro-apoptotic activated caspase-3 and Bax, and upregulation of anti-apoptotic Bcl-2, thereby mitigating apoptotic morphological alterations. DPN pre-treatment decreased the expression levels of pro-inflammatory cytokines IL-1β and IL-6 through attenuation of Aβ1-42-induced phosphorylation of mitogen-activated protein kinases JNK and p38. In addition, DPN enhanced ERK1/2 and Akt phosphorylation depressed by Aβ1-42. These findings suggest that DPN protects neurons from Aβ1-42-induced neurotoxicity through a variety of mechanisms, ranging from anti-oxidation, anti-apoptosis, through to anti-inflammation. © 2014 Elsevier Ireland Ltd.Mahidol UniversityNeuroscienceArticleSCOPUS10.1016/j.neulet.2014.06.029