Protective effects of perilla oil and alpha linolenic acid on SH-SY5Y neuronal cell death induced by hydrogen peroxide

Abstract

BACKGROUND/OBJECTIVEOxidative stress plays a key role in neuronal cell damage, which is associated with neurodegenerative disease. The aim of present study was to investigate the neuroprotective effects of perilla oil (PO) and its active component, alpha-linolenic acid (ALA), against hydrogen peroxide (H2O2)-induced oxidative stress in SH-SY5Y neuronal cells.MATERIALS/METHODSThe SH-SY5Y human neuroblastoma cells exposed to 250 µM H2O2 for 24 h were treated with different concentrations of PO (25, 125, 250 and 500 µg/mL) and its major fatty acid, ALA (1, 2.5, 5 and 25 µ/mL). We examined the effects of PO and ALA on H2O2-induced cell viability, lactate dehydrogenase (LDH) release, and nuclear condensation. Moreover, we determined whether PO and ALA regulated the apoptosis-related protein expressions, such as cleaved-poly ADP ribose polymerase (PARP), cleaved caspase-9 and -3, BCL-2 and BAX.RESULTSTreatment of H2O2 resulted in decreased cell viability, increased LDH release, and increase in the nuclei condensation as indicated by Hoechst 33342 staining. However, PO and ALA treatment significantly attenuated the neuronal cell death, indicating that PO and ALA potently blocked the H2O2-induced neuronal apoptosis. Furthermore, cleaved-PARP, cleaved caspase-9 and -3 activations were significantly decreased in the presence of PO and ALA, and the H2O2-mediated up-regulated BAX/BCL-2 ratio was blocked after treatment with PO and ALA.CONCLUSIONSPO and its main fatty acid, ALA, exerted the protective activity from neuronal oxidative stress induced by H2O2. They regulated apoptotic pathway in neuronal cell death by alleviation of BAX/BCL-2 ratio, and down-regulation of cleaved-PARP and cleaved caspase-9 and -3. Although further studies are required to verify the protective mechanisms of PO and ALA from neuronal damage, PO and ALA are the promising agent against oxidative stress-induced apoptotic neuronal cell death.

Perilla Oil Alleviates High-Fat Diet-Induced Inflammation in the Colon of Mice by Suppressing Nuclear Factor-Kappa B Activation

“…Similar to previous reports, the fatty acid composition analysis of PO used in our study showed that a-linolenic acid was in the highest amount (59.5%, omega-3 fatty acid), followed by oleic acid (14.2%, monounsaturated fatty acid), linoleic acid (12.3%, omega-6 fatty acid), and palmitic acid (5.8%, saturated fatty acid). 28,29 The main fatty acids present in FO used in this study were EPA (15%, omega-3 fatty acid), DHA (15%, omega-3 fatty acid), palmitic acid (20%, saturated fatty acid), palmitoleic acid (14%, monounsaturated fatty acid), oleic acid (12%, monounsaturated fatty acid), linoleic acid (<3%, omega-6 fatty acid), and linolenic acid (<3%, omega-3 fatty acid).…”

Twelve-Month Studies on Perilla Oil Intake in Japanese Adults—Possible Supplement for Mental Health

“…Because of the positive impact of LNA's metabolites, such as eicosapentaenoic acid (EPA) and DHA, on learning-related memory in young and old rats [10,24] as well as Alzheimer's disease (AD) in model rats [25,26], linoleic acid (LLA), being the precursor of EPA and DHA, is also gaining increasing interest for improving brain cognition. Direct application of purified LNA to glial cell lines inhibited Amyloid β-induced oxidative stress [27]. Neuronal cell lines pretreated with LNA also inhibited H 2 O 2 -induced apoptotic neuronal cell death [28], thus suggesting that LNA has significant antioxidative potential.…”

Neuroprotective effect ofAster yomena(Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

“…It was reported that H 2 O 2 activated nuclear translocation of nuclear factor-kappa B (NF-κB) in SH-SY5Y cells and it up-regulated COX-2 and inducible nitric oxide synthase (iNOS) in the inflammatory pathway [26]. Our previous study also demonstrated that H 2 O 2 activated apoptosis pathway in SH-SY5Y cells and several therapeutic agents reduced the cell death [5].…”

“…Oxidative stress is generated in living organisms when the homeostasis between the production of free radicals and antioxidant defense system gets out of balance [4]. Previous studies demonstrated that oxidative stress exerts cellular damage including DNA injury, inflammation, and apoptosis of brain cells including neuronal, glial, and cerebrovascular cells [5][6][7]. High concentrations of reactive oxygen species (ROS) can cause damage to cellular lipids, proteins, and DNA because of strong reactivity [8].…”