![]() ![]() observed in human SH SY5Y neuroblastoma cells, a cellular model for AD, that TQ showed a lowered amyloid β oxidation and a decreased nitric oxide level as a result of the antioxidative capacity of TQ. For example, Kandeil and his colleagues postulated that the beneficial effect of TQ against cisplatin-induced neurotoxicity is due to its antioxidant activity. The neuroprotective effects of TQ are often attributed to its antioxidative effects. Likewise, in Alzheimer’s disease (AD), cell degeneration seems to be related to inflammation and oxidative stress. In Parkinson’s disease (PD), for instance, oxidative stress is considered to be one of the main reasons for the decline of the dopaminergic neurons, besides the aggregation of α-synuclein and the induction of inflammation. Neurodegenerative disorders are often caused or accompanied by oxidative stress. Based on a study by Badary et al., the protective properties of TQ have been attributed partially to its ability to scavenge superoxide radicals ex vivo. Besides the use of TQ throughout the centuries, it has been also reported that TQ may be an effective compound in neurodegenerative disease models. Recently, several publications about TQ and its effects against COVID-19 have been published, which reflect the high expectations placed on TQ. The promising pharmacological potential of TQ is still part of scientific curiosity, which is demonstrated by the increasing number of publications related to new and primarily unexpected pharmacological activity. While Nigella sativa seeds were used in the past as a natural treatment to support health and cure illnesses, modern studies demonstrate that TQ has anti-bacterial, anti-inflammatory, and anti-cancer activities. Nigella sativa seeds, as well as its main pharmacologically active compound, thymoquinone (TQ) (2-isopropyl-5-methyl-1,4-benzoquinone), have been widely used in traditional medicine for several thousand years. Our study provides evidence that TQ has no direct scavenging effect on superoxide radicals. The described anti-cancer ability of TQ might be a result of the pro-apoptotic condition in neuroblastoma cells. Therefore, the enhanced resistance against oxidative stress in primary cell culture might be a consequence of a lowered caspase-3 activity combined with an increased pool of reduced glutathione. Evaluation of the glutathione level revealed an increased level of total glutathione in both cell culture systems. On the contrary, TQ itself tremendously increased the caspase-3 activity in the neuroblastoma cell line. In mesencephalic cell culture under oxidative stress conditions, caspase-3 activity was decreased when TQ was administered. Additionally, the total ROS levels were unaltered. Measurements in both cell culture systems revealed that the mitochondrial membrane potential was tendentially lowered, while ATP production was mostly unaffected. Quantification of the formation of superoxide radicals via electron paramagnetic resonance showed an initial increase in the level of superoxide radicals in the cell by TQ. Tyrosine hydroxylase staining revealed that TQ significantly protected dopaminergic neurons and preserved their morphology under oxidative stress conditions. The effects of TQ were studied in models with mitochondrial impairment and oxidative stress induced by rotenone in N18TG2 neuroblastoma cells and rotenone/MPP + in primary mesencephalic cells. Therefore, the present study was designed to reassess the radical scavenging properties of TQ and explore a potential mode of action. Thymoquinone (TQ), an active compound from Nigella sativa seeds, is often described as a pharmacologically relevant compound with antioxidative properties, while the synthesis of TQ in the plant via oxidations makes it inapplicable for scavenging radicals.
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