Abstract
BackgroundApoptosis is often the end result of oxidative damage to neurons. Due to shared pathways between oxidative stress, apoptosis and antioxidant defence systems, an oxidative insult could end up causing cellular apoptosis or survival depending on the severity of the insult and cellular responses. Plant bioresources have received close attention in recent years for their potential role in regulating the pathways involved in apoptosis and oxidative stress in favour of cell survival. Rice bran is a bioactive-rich by-product of rice milling process. It possesses antioxidant properties, making it a promising source of antioxidants that could potentially prevent oxidative stress-induced neurodegenerative diseases.MethodsThus, the present study investigated the neuroprotective properties of oryzanol-rich fraction (ORF) against hydrogen peroxide (H2O2)-induced neurotoxicity in differentiated human neuroblastoma SH-SY5Y cells. ORF was extracted from rice bran using a green technology platform, supercritical fluid extraction system. Furthermore, its effects on cell viability, morphological changes, cell cycle, and apoptosis were evaluated. The underlying transcriptomic changes involved in regulation of oxidative stress, apoptosis and antioxidant defence systems were equally studied.ResultsORF protected differentiated SH-SY5Y cells against H2O2-induced neurotoxicity through preserving the mitochondrial metabolic enzyme activities, thus reducing apoptosis. The mechanistic basis for the neuroprotective effects of ORF included upregulation of antioxidant genes (catalase, SOD 1 and SOD 2), downregulation of pro-apoptotic genes (JNK, TNF, ING3, BAK1, BAX, p21 and caspase-9), and upregulation of anti-apoptotic genes (ERK1/2, AKT1 and NF-Kβ).ConclusionThese findings suggest ORF may be an effective antioxidant that could prevent oxidative stress-induced neurodegenerative disorders.
Highlights
Apoptosis is often the end result of oxidative damage to neurons
The protective effects of oryzanol-rich fraction (ORF) against Hydrogen peroxide (H2O2)-induced cell death were further corroborated by flow cytometric analyses, which indicated that ORF reduced the apoptotic and necrotic cells’ population in SH-SY5Y cells
Our results showed that H2O2 induced Jun N-terminal kinases (JNK) and caspase-9 activation, which were both attenuated by ORF treatment, suggesting that the protective effects of ORF against H2O2-induced injury in SH-SY5Y cells were partly mediated through its protection of the mitochondria
Summary
Apoptosis is often the end result of oxidative damage to neurons. Due to shared pathways between oxidative stress, apoptosis and antioxidant defence systems, an oxidative insult could end up causing cellular apoptosis or survival depending on the severity of the insult and cellular responses. Rice bran is a bioactive-rich by-product of rice milling process It possesses antioxidant properties, making it a promising source of antioxidants that could potentially prevent oxidative stress-induced neurodegenerative diseases. Superoxide anions, hydrogen peroxide (H2O2) and the hydroxyl radical have been indicated as potent mediators of neuronal oxidative stress [2] They elicit a complex cascade of events that may eventually remove the initiating stimulus or result in apoptotic death of the cells, depending on the severity of the damage [1]. MAPKs encompass a large number of serine/threonine kinases involved in regulating cellular processes including proliferation, differentiation, stress adaptation, and apoptosis. These include the extracellular signal-regulated kinases (ERK), the c-Jun N-terminal kinases (JNK), and the p38 kinases. The ERK pathway is linked to the regulation of cell proliferation, while the JNK and p38 pathways are more strongly tied to stress [1]
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