Neuroprotective effect of taurine on human neuroblastoma under induced stress

Abstract

Background High concentrations of hydrocortisone is known to cause oxidative stress in neural cell, impairing damage repair and, consequently, triggering cell death. This represents one of the mechanisms of Alzheimer's Disease (AD). To prevent oxidative stress, novel studies have demonstrated neuroprotective effects of taurine in specific concentrations, regulating brain activity, maintaining the integrity of neural membrane and controlling calcium homeostasis, thus preventing cell death by preventing oxidative stress. Method First, SH‐SY5Y (human neuroblastoma) cells were incubated with different concentrations of taurine (0.25 to 1 mg/mL), then, after 24h, cells were exposed to 200 µM of hydrocortisone for another 24h (a stablished concentration that reduces SH‐SY5Y viability and induces oxidative stress). Cell viability was evaluated by crystal violet technique. Cells not exposed to hydrocortisone or taurine were used as control. Result A concentration curve of taurine was performed (0.25 to 1 mg/mL), demonstrating that the compound stimulates SH‐SY5Y cell growth at 0.5 mg/mL (p = 0.0457) (Figure 1A). This concentration was stablished as protective. To verify the neuroprotective potential, cells were pre‐treated with 0.5 mg/mL of taurine and then exposed to 200 µM of hydrocortisone. Importantly, cytoviability was not only preserved but also statistically improved, compared to the control group (p < 0.0001) (Figure 1B). Conclusion In high concentration (200 µM), hydrocortisone induces oxidative stress in SH‐SY5Y, an important pathway observed in AD. Once cells are pre‐incubated with 0.5 mg/mL of taurine followed by 200 µM of hydrocortisone exposure, cytoviability is preserved and stimulated, representing a considerable step to further evaluate taurine as a significant neuroprotective tool for AD. (1) Moraes, C.D.G.O. et al. Genotoxic effects of photodynamic therapy in laryngeal cancer cells–An in vitro study. Experimental Biology and Medicine, v. 244, n. 3, p. 262‐271, 2019. (2) Salles, G.N. et al. Prolonged Drug‐Releasing Fibers Attenuate Alzheimer’s Disease‐like Pathogenesis. ACS applied materials & interfaces, v.10, n.43, p.36693‐36702, 2018. (3) Sergeeva, O.A. et al. Taurine‐induced long‐lasting enhancement of synaptic transmission in mice: Role oftransporters. The Journal of physiology, v.550, n.3, p.911‐919, 2003. (4) ROSSATO, R.C. et al. Hydrocortisone cytorestores oxidative stress‐induced neuroblastoma. Alzheimer's & Dementia: The Journal of the Alzheimer's Association, 15(7), p.642, 2019.