Photodynamic therapy provides the formation of reactive oxygen species that are capable of inducing cell death. Human laryngeal carcinoma (HEp-2) cells have been evaluated in this study under PDT treatment. Cells were treated with photosensitizer aluminum phthalocyanine tetrasulfonate (AlPcS4) and irradiated with a Biopdi/Irrad-Led5 660 LED with 660 nm wavelength, intensity of delivered light of 25 mW/cm2, power of 70 mW, fluence of 5 J/cm2 for 24 h and 48 h, and then evaluated. Cell population was not increased by PDT treatment after the tested period. The apoptosis assay demonstrated that control groups exhibit approximately 60% of living cells in the 24 h and 48 h periods, however. A significant increase in apoptotic cells was observed after the photodynamic therapy treatments, for both 24 and 48 h groups. Over 50% of cells were under apoptosis after photodynamic therapy, evidencing a death process generated from the oxidative damage of the treatment. Comet assay and micronucleus assessments, both of which evaluate genotoxicity, demonstrated favorable results to damages caused by the photodynamic therapy treatment. Thus, photodynamic therapy is proposed to damage nuclear cells and the subcellular structure of carcinogenic cells. Impact statement Recently, the use of photodynamic therapy grows as an alternative treatment for cancer, since it has a noninvasive characteristic and affinity to the tumor tissue. Accordingly, understanding the therapy’s foci of action is important for the technique improvement. This work aims to understand the genotoxic effect triggered by the therapy action, thus evidencing the permanent changes caused to the genetic material of the tumor cell after the treatment. Therefore, to increase the knowledge in this study field, the methodology of the comet assay and count of micronucleus formed after the therapy was adopted in order to understand if the damage caused to the DNA of tumor cell makes its replication process unfeasible in future generations. The study allows a better therapeutic approach to the cancer treatment, making the process of association between therapies a more effective option during the disease treatment.
Alzheimer's disease (AD) is the most common, progressive and irreversible neurodegenerative disorder, characterized by memory loss, cognitive impairment and behavioral abnormalities. Although there is no cure, several study strategies seek to elucidate mechanisms of the disease. Recent studies address the benefits of taurine. Thus, the present study aims to analyze neuroprotective effects of taurine in human neuroblastoma (SH-SY5Y), using an in vitro experimental model of oxidative stress induced by hydrocortisone. This work showed for the first time that taurine can promote neuroprotection in SH-SY5Y under oxidative stress caused by hydrocortisone. Cell viability was evaluated using crystal violet and the evaluation of cell morphology was performed by scanning electron microscopy (SEM). The viability of SH-SY5Y pre-treated with taurine and stressed with hydrocortisone was preserved, compared to the stressed only group, which was also morphologically observed. Therefore, taurine can represent a considerable therapeutic candidate in the prevention of neurodegenerative diseases, such as AD.
Alzheimer’s disease (AD) is a type of dementia that affects millions of people. Although there is no cure, several study strategies seek to elucidate the mechanisms of the disease. Recent studies address the benefits of taurine. Thus, the present study aims to analyze the neuroprotective effect of taurine on human neuroblastoma, using an in vitro experimental model of oxidative stress induced by hydrocortisone in the SH-SY5Y cell line as a characteristic model of AD. The violet crystal assay was used for cell viability and the evaluation of cell morphology was performed by scanning electron microscopy (SEM). After pretreatment with taurine, the SH-SY5Y cell showed an improvement in cell viability in the face of oxidative stress and improved cell morphology. Thus, the treatment presented a neuroprotective effect.GRAPHICAL ABSTRACT
A Doença de Alzheimer é um tipo de demência que acomete milhões de pessoas, sendo responsável por 60% de todos os casos de doenças neurodegenerativas. Embora não tenha cura, diversas estratégias de estudo vêm sendo desenvolvidas a fim de elucidar os mecanismos da doença. Estudos recentes abordam os benefícios do cortisol em aspectos imunológicos, musculares, renais, respostas inflamatórias e até mesmo em patologias neurodegenerativas. A hidrocortisona é um medicamento sintético utilizado para simular o cortisol. Deste modo, o estudo explora os efeitos da hidrocortisona na senescência neural, objetivando analisar seu efeito neuroprotetor. Assim, desenvolveu-se um modelo experimental in vitro de estresse oxidativo, induzido por peróxido de hidrogênio na linhagem celular Neuro-2a (Neuroblastoma de Murino) a fim de simular aspectos característicos da Doença de Alzheimer. Foram então realizados experimentos de viabilidade e morfologia celular. A hidrocortisona em baixa concentração promoveu aumento na viabilidade celular, enquanto que o peróxido de hidrogênio diminuiu a viabilidade celular, ocorrendo o efeito de estresse oxidativo. No aspecto morfológico, a hidrocortisona preservou os prolongamentos das células, já o peróxido de hidrogênio fez com que os prolongamentos retraíssem, assim perdendo as sinapses. Com os resultados obtidos, pode-se concluir que a hidrocortisona preservou a célula neural do efeito do estresse oxidativo.
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.
Proteínas de choque térmico (HSP) são moléculas intracelulares multifuncionais que, eventualmente, podem estar envolvidas na malignização celular. Terapia fotodinâmica (TFD) pode levar à redução do tumor e vasos sanguíneos ao redor. Objetivo foi avaliar ação da TFD sobre as HSPs em células neoplásicas de carcinoma de laringe humana (HEp-2). As células foram irradiadas com LED a 660 nm, 5 J/cm2, 70 mW, por 3 minutos e 20 segundos; incubadas por períodos de 24, 48 e 72 horas; após os períodos de incubação foi realizada a extração de proteínas e corrido gel de poliacrilamida para avaliação das proteínas por Western-Blotting. As células foram imunomarcadas com anticorpos anti-HSP27, anti-HSP70 e anti-HSP90 e analisadas no microscópio confocal. A viabilidade celular foi avaliada pelo teste de cristal violeta. No gel de poliacrilamida foram identificadas bandas próximas a 27 kDa, 70 kDa e 90 kDa. Nas fotomicrografias observou-se redução do número de células após TFD, comprovado por teste de viabilidade (cristal violeta); e intensa marcação de HSPs após TFD, principalmente próximas ao núcleo. Concluiu-se que HSP27, HSP70 e HSP90 são muito produzidas em células HEp-2. TFD foi eficaz devido à redução do número de células e considerada opção viável para o tratamento dessa doença. Embora seja relatada a participação das HSPs 27, 70 e 90 como protetoras das células tumorais, nossos resultados indicam que a TFD ativa tais proteínas para a redução das células tumorais.
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