Fimbristylis ovata extract and its ability to encounter AGEs-induced neurotoxicity in SH-SY5Y

Toxicol Res. 2021 Jan 25;37(3):355-367. doi: 10.1007/s43188-020-00072-z. eCollection 2021 Jul.

Abstract

Abstract: Advanced glycation end products (AGEs) upon binding to its receptor (receptor for AGEs, RAGE) trigger several pathological processes involving oxidative stress and inflammatory pathway which play a pivotal role in various degenerative diseases including Alzheimer's disease. Fimbristylis ovata (F. ovata) has long been reported to be used as a traditional herbal medicine; nonetheless, very few studies have been reported. In this study, the protective effects of F. ovata extract on neurotoxicity of hippocampal neuronal cells (SH-SY5Y) was investigated. When compared to normal control, AGEs treatment significantly induced oxidative stress level and enhanced NF-κB translocation to nucleus in the neuronal cells (p < 0.05). The increase in NF-κB translocation leads to increase in transcription level of the target genes including RAGE and pro-inflammatory cytokines which include interleukin 1 beta (IL1B), tumor necrosis factor-alpha (TNFA) and interleukin 6 (IL6). Pre-treatment of SH-SY5Y with the extracts of F. ovata shows favorable results by significantly suppressing oxidative stress level (p < 0.05) as well transcriptional level of RAGE (p < 0.05) and pro-inflammatory cytokines (p < 0.05). Chemical analysis of F. ovata extracts using High Resolution Liquid Chromatograph Mass Spectrometer (HR-LCMS) and Gas Chromatograph with high resolution Mass Spectrometer (GC-HRMS) suggested some potential active phytochemical compounds. The results from this study may provide possible alternative treatment for prevention and/or therapy of neurodegenerative disorders by targeting the above-mentioned pathways. The role of the phytochemical active ingredient (s) in inhibiting the AGEs-triggered signaling inflammatory pathway should be investigated in future study.

Keywords: Fimbristylis ovata; Neurotoxicity; Oxidative stress; Pro-inflammatory cytokines; SH-SY5Y.