纳米粒减弱高糖诱导的HepG2细胞氧化损伤

M. Shokrzadeh, Hakim H Abdi, Azin Asadollah-Pour, F. Shaki
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引用次数: 11

摘要

目的高血糖是糖尿病常见的代谢紊乱,可导致氧化损伤。抗氧化剂的使用有利于控制和预防糖尿病的副作用。本研究旨在评价纳米粒作为抗氧化剂对人肝细胞肝癌细胞系(HepG2)中葡萄糖诱导的细胞毒性、活性氧(ROS)、脂质过氧化(LPO)和谷胱甘肽(GSH)含量的影响。材料与方法在本实验研究中,我们将HepG2细胞分为两组:1 .经5 mM d -葡萄糖处理的细胞(对照组);用45 mM D-甘露醇+5 mM D-葡萄糖(渗透控制)处理的细胞;用50mm d -葡萄糖(高糖)处理的细胞,和用50mm d -葡萄糖+纳米粒处理的细胞。测定细胞活力、ROS形成、LPO和GSH,并进行统计学分析。结果高糖(50 mM)处理导致HepG2细胞明显死亡,氧化应激标志物升高。有趣的是,浓度为50 mM的纳米粒显著降低高糖诱导的细胞毒性、ROS形成和LPO。该浓度的纳米粒使HepG2细胞GSH含量升高(P<0.05)。结论纳米微球的抗氧化特性使其成为抑制不同器官高血糖氧化损伤的理想候选物质。
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Nanoceria Attenuated High Glucose-Induced Oxidative Damage in HepG2 Cells
Objective Hyperglycemia, a common metabolic disorder in diabetes, can lead to oxidative damage. The use of antioxidants can benefit the control and prevention of diabetes side effects. This study aims to evaluate the effect of nanoceria particles, as an antioxidant, on glucose induced cytotoxicity, reactive oxygen species (ROS), lipid peroxidation (LPO) and glutathione (GSH) content in a human hepatocellular liver carcinoma cell line (HepG2) cell line. Materials and Methods In this experimental study, we divided HepG2 cells into these groups: i. Cells treated with 5 mM D-glucose (control), ii. Cells treated with 45 mM D- mannitol+5 mM D-glucose (osmotic control), iii. Cells treated with 50 mM D-glucose (high glucose), and iv. Cells treated with 50 mM D-glucose+nanoceria. Cell viability, ROS formation, LPO and GSH were measured and analyzed statistically. Results High glucose (50 mM) treatment caused significant cell death and increased oxidative stress markers in HepG2 cells. Interestingly, nanoceria at a concentration of 50 mM significantly decreased the high glucose-induced cytotoxicity, ROS formation and LPO. This concentration of nanoceria increased the GSH content in HepG2 cells (P<0.05). Conclusion The antioxidant feature of nanoceria particles makes it an attractive candidate for attenuation of hyperglycemia oxidative damage in different organs.
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