Protective Effect of Trehalose Against H2O2-induced Cytotoxicity and Oxidative Stress in PC-12 Cell Line and the Role of Heat Shock Protein-27

Q4 Pharmacology, Toxicology and Pharmaceutics
Akram Norouzi, N. Ziamajidi, Asie Sadeghi, Mahdieh Nazari-Robati
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Abstract

Background: Oxidative stress has been shown to be an important factor, which plays a significant role in the pathogenesis of neurodegenerative disorders. Heat Shock Protein-27 (HSP-27) has been implicated in antioxidant responses against oxidative stress. Trehalose is a natural disaccharide widely used in a variety of food products with demonstrated protective effects against several neurodegenerative diseases. This study investigated the effects of trehalose on antioxidant responses, and the gene expressions for HSP-27 and caspase-3 against hydrogen peroxide (H2O2) induced oxidative injury in PC-12 cell line. Methods: The PC-12 cells were treated with various concentrations of H2O2 and trehalose for 24hr. The cell viability was assessed, using MTT and Lactate Dehydrogenase (LDH) release assays. Moreover, the activity of Catalase (CAT) and Glutathione Peroxidase (GPx) enzymes, and the Malondialdehyde (MDA) levels were determined. In addition, the levels of HSP-27 and caspase-3 gene expressions were measured. Results: The results indicated that the pretreatment with trehalose increased cell survival against the H2O2-induced oxidative injury. Furthermore, trehalose elevated the CAT and GPx activities and reduced MDA levels compared to that of control group (P˂0.05). Moreover, trehalose upregulated the HSP-27 gene expression, while reducing the expression of caspase-3 gene compared to that of the untreated cells (P˂0.05). All of these biochemical changes were found to be dose-dependent for trehalose. Conclusion: Based on the study findings, trehalose had the capacity to attenuate the oxidative stress and cell injury. Therefore, trehalose may be suggested as a therapeutic agent to treat neurodegenerative disorders caused by oxidative stress damages.
海藻糖对h2o2诱导的PC-12细胞毒性和氧化应激的保护作用及热休克蛋白27的作用
背景:氧化应激已被证明是一个重要因素,在神经退行性疾病的发病机制中发挥着重要作用。热休克蛋白-27(HSP-27)与对抗氧化应激的抗氧化反应有关。海藻糖是一种天然双糖,广泛用于各种食品中,对几种神经退行性疾病具有保护作用。本研究研究了海藻糖对PC-12细胞抗氧化反应的影响,以及HSP-27和胱天蛋白酶-3对过氧化氢(H2O2)诱导的PC-12细胞氧化损伤的基因表达。方法:用不同浓度的H2O2和海藻糖处理PC-12细胞24小时。使用MTT和乳酸脱氢酶(LDH)释放测定法评估细胞活力。此外,还测定了过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性以及丙二醛(MDA)的水平。此外,还测定了HSP-27和胱天蛋白酶-3基因的表达水平。结果:海藻糖预处理提高了细胞对H2O2诱导的氧化损伤的存活率。此外,与对照组相比,海藻糖提高了CAT和GPx活性,降低了MDA水平(P 0.05)。此外,与未处理的细胞相比,海藻糖上调了HSP-27基因的表达,同时降低了胱天蛋白酶-3基因的表达(P 0.05。结论:根据研究结果,海藻糖具有减轻氧化应激和细胞损伤的能力。因此,海藻糖可能被建议作为治疗剂来治疗由氧化应激损伤引起的神经退行性疾病。
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来源期刊
Iranian Journal of Toxicology
Iranian Journal of Toxicology Environmental Science-Health, Toxicology and Mutagenesis
CiteScore
1.60
自引率
0.00%
发文量
24
审稿时长
9 weeks
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