Protective effects of perilla oil and alpha linolenic acid on SH-SY5Y neuronal cell death induced by hydrogen peroxide.
- Author:
Ah Young LEE
1
;
Ji Myung CHOI
;
Myoung Hee LEE
;
Jaemin LEE
;
Sanghyun LEE
;
Eun Ju CHO
Author Information
- Publication Type:Original Article
- Keywords: alpha-linolenic acid; apoptosis; hydrogen peroxide; neuroprotective effect; perilla
- MeSH: Adenosine Diphosphate Ribose; alpha-Linolenic Acid*; Apoptosis; Caspase 9; Cell Death*; Cell Survival; Down-Regulation; Humans; Hydrogen Peroxide*; Hydrogen*; L-Lactate Dehydrogenase; Neuroblastoma; Neurodegenerative Diseases; Neurons*; Neuroprotective Agents; Oxidative Stress; Perilla*
- From:Nutrition Research and Practice 2018;12(2):93-100
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/OBJECTIVE: Oxidative 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/METHODS: The 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. RESULTS: Treatment 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. CONCLUSIONS: PO 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.
