Neuroprotective effect of hydrocortisone on human glioblastoma under H2 O2 -induced stress
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2021-12-01
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Rossato, Rafaella Carvalho
Pinto, Jessica Cristina
de Oliveira Moraes, Carlos Dailton Guedes [UNESP]
Salles, Geisa Nogueira
Pacheco-Soares, Cristina
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BACKGROUND: In Alzheimer's disease (AD), oxidative stress is considered one of the major roles in the pathophysiologic process, increasing reactive oxygen species (ROS), causing an imbalance that may initiate and enhance the disease. The reduction of hydrogen peroxide (H2 O2 ) produces ROS, resulting in brain tissue damage and disruption of brain cells repair. According to recent studies, at low concentrations, hydrocortisone possesses neuroprotective and restorative properties, representing a potential tool for AD treatment. In this study, we identify neuropreventive effects of hydrocortisone on oxidative damage caused by H2 O2 in human glioblastoma (A172). METHOD: A172 cells were cultivated and pretreated with 100 μM of hydrocortisone for 24h. Then, cells were stressed with 2.5mM of H2 O2 for another 24h. Cell viability was evaluated by crystal violet technique and cells morphology was assessed by scanning electron microscopy (SEM). Cells not incubated with hydrocortisone nor exposed to H2 O2 were used as control. RESULT: As seen in figure 1, when A172 cells are exposed to H2 O2 , cytoviability is significantly reduced, compared to the control group (p <0.0001). When in contact with hydrocortisone, A172 cells viability is maintained similar to the control group. However, when A172 cells are pretreated with hydrocortisone and stress with H2 O2 , cytoviability is significantly preserved, compared to the stressed-only group (p <0.0001). In other words, hydrocortisone plays a cytoprotective role in A172 H2 O2 -exposed cells. Figure 2 corroborates this result, demonstrating cell morphology at 100x and 1000x magnifications. At 100x magnification, cell population of the pretreated and stressed group is greater than the H2 O2 -exposed group. At 1000x, pretreated cells projections were morphologically preserved in comparison to the H2 O2 -exposed only group. CONCLUSION: Our previous results indicate that hydrocortisone neurorestores impaired human neuroblastoma, now we demonstrate that human glioblastoma are also preserved with hydrocortisone against the toxicity caused by the oxidative stress induced by H2O2. Further analysis are being performed to better elucidate the process. HAM, Sangwoo et al. Hydrocortisone-induced parkin prevents dopaminergic cell death via CREB pathway in Parkinson's disease model. References: (1) Scientific reports, v. 7, n. 525, p. 1- 13, 2017. (1) Rossato, Rafaella Carvalho, et al. Hydrocortisone cytorestores oxidative stress-induced neuroblastoma. Alzheimer's & Dementia 15 (2019): P642-P642.
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Alzheimer's & dementia : the journal of the Alzheimer's Association, v. 17, p. e052678-.