BLACK CUMIN SEED (NIGELLA SATIVA LINN.) OIL AND ITS FRACTIONS PROTECT AGAINST BETA AMYLOID PEPTIDE‐INDUCED TOXICITY IN PRIMARY CEREBELLAR GRANULE NEURONS

Abstract

The neuroprotective effect of Nigella sativa oil (NSO) and its fractions against beta amyloid (Aβ)-induced cell death in primary rat cerebellar granule neurons was investigated. Primary cultures were pretreated for 5 h with NSO and its fractions – hexane fraction (HF), ethyl acetate fraction (EAF) and water fraction (WF) – before incubating with 10 µM Aβ1-40 for 24 h. Cell viability was investigated using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS) and lactate dehydrogenase (LDH) assays. Results of the MTS assay showed that the WF and NSO were significantly protective against cell death induced by 10 µM Aβ1-40 at 1, 10 and 100 µg/mL probably because of antioxidant properties as determined by 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical trapping method. HF and EAF had low DPPH scavenging effect and were only effective at 100 µg/mL. However, NSO and its fractions were weakly protective against cell membrane damage in the LDH assay. NSO and its fractions, especially the WF, may play a role in the prevention of Aβ-induced cell death. PRACTICAL APPLICATIONS Neurodegeneration in Alzheimer's disease (AD) has been associated with the toxic effects of beta amyloid (Aβ), a by-product of amyloid precursor protein. Natural products that are able to reduce Aβ-induced neurotoxicity are candidates for preventing as well as for treating this neurodegenerative condition. Thus, the neuroprotective effects of Nigella sativa against Aβ toxicity may play a potential role in preventing AD progression.