Safranal protects against ischemia-induced PC12 cell injury through inhibiting oxidative stress and apoptosis
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ORIGINAL ARTICLE
Safranal protects against ischemia-induced PC12 cell injury through inhibiting oxidative stress and apoptosis Fatemeh Forouzanfar 1,2 & Elham Asadpour 3 & Hossein Hosseinzadeh 4 & Mohammad Taher Boroushaki 5 & Afrouz Adab 6 & Seyedeh Hoda Dastpeiman 7 & Hamid R. Sadeghnia 5,6,7 Received: 6 February 2020 / Accepted: 11 October 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Safranal, isolated from saffron (Crocus sativus L.), is known to possesses neuroprotective effects. In this study, the neuroprotective potential of safranal against PC12 cell injury triggered by ischemia/reperfusion was investigated. PC12 cells were pretreated with safranal at concentration ranges of 10–160 μM for 2 h and then deprived from oxygen-glucose-serum for 6 h, followed by reoxygenation for 24 h (OGD condition). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), 2,7-dichlorofluorescin diacetate (DCF-DA), and comet assays were used to measure the extent of cellular viability, reactive oxygen substances (ROS), and DNA damage, respectively. Also, propidium iodide (PI) flow cytometry assay and western blotting of bax, bcl-2, and cleaved caspase-3 were performed for assessment of apoptosis. OGD exposure reduced the cell viability and increased intracellular ROS production, oxidative DNA damage, and apoptosis, in comparison with untreated control cells. Pretreatment with safranal (40 and 160 μM) significantly attenuated OGD-induced PC12 cell death, oxidative damage, and apoptosis. Furthermore, safranal markedly reduced the overexpression of bax/bcl-2 ratio and active caspase-3 following OGD (p < 0.05). The present findings indicated that safranal protects against OGD-induced neurotoxicity via modulating of oxidative and apoptotic responses. Keywords Safranal . Crocus sativus . Oxygen-glucose-serum deprivation (OGD) . Ischemia . Apoptosis . Comet assay
Introduction Ischemic cerebrovascular diseases are one of the most important causes of morbidity and death, globally. In the context of lack of effective therapy, the demand for useful stroke therapy is imperative (Cassella and Jagoda 2017; Zhou et al. 2017;
Paliwal et al. 2018; Thieme et al. 2018). Various methods have been used to improve our understanding of stroke and also to identify anti-stroke components (Wang et al. 2014). Numerous animal models have been examined in this context although they usually result in the wasting of significant amounts of human and material resources (Liu et al. 2017).
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00210-020-01999-8) contains supplementary material, which is available to authorized users. * Hamid R. Sadeghnia [email protected] 1
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
2
Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
3
Anaestehsiology and Critical Care Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
4
Ph
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