{'fraction_non_alphanumeric': 0.027510316368638238, 'fraction_numerical': 0.011691884456671253, 'mean_word_length': 6.311557788944723, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Palmitate induced ER stress‐mediated neurotoxicity in SH‐SY5Y cells

Recent studies have indicated an association between obesity and neurodegenerative disease including Alzheimer's disease. Palmitate, a representative circulating saturated fatty acid in obese patient, is considered as a candidate mediator of neurotoxicity as in peripheral tissues. Therefore, we investigated the underlying mechanism involved in palmitate‐induced lipotoxicity using SH‐SY5Y human neuroblastoma cells. Palmitate treatment significantly increased caspase‐3 activity and apoptotic body staining. Endoplasmic reticulum (ER) stress was significantly induced by palmitate reflected in the increased mRNA level of spliced X box‐binding protein‐1. Palmitate activated c‐jun N terminal kinase, a known mediator of apoptosis and tau phosphorylation in response to ER stress, resulting in tau hyperphosphorylation in SH‐SY5Y cells. Palmitate significantly repressed the phosphorylation of AMP‐activated protein kinase and acetyl‐CoA carboxylase, suggesting an impairment in fatty acid oxidation. However, we did not observe the significant change in protein kinase B (Akt) phosphorylation in cells treated with palmitate. These findings indicate that palmitate induces ER stress‐mediated neurotoxicity, but does not attenuate insulin signaling pathway by inhibiting Akt activity in SH‐SY5Y cells. This work was supported by a grant from Korea Research Foundation (#2009‐0069120).