Shokrzadeh Mohammad, Abdi Hakimeh, Asadollah-Pour Azin, Shaki Fatemeh
Pharmaceutical Science Research Center, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran; Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.
Department of Toxicology and Pharmacology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.
Cell J. 2016 Spring;18(1):97-102. doi: 10.22074/cellj.2016.3992. Epub 2016 Apr 4.
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.
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.
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).
The antioxidant feature of nanoceria particles makes it an attractive candidate for attenuation of hyperglycemia oxidative damage in different organs.
高血糖是糖尿病常见的代谢紊乱,可导致氧化损伤。使用抗氧化剂有助于控制和预防糖尿病的副作用。本研究旨在评估纳米氧化铈颗粒作为抗氧化剂对人肝癌细胞系(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。
在本实验研究中,我们将HepG2细胞分为以下几组:i. 用5 mM D-葡萄糖处理的细胞(对照组);ii. 用45 mM D-甘露醇+5 mM D-葡萄糖处理的细胞(渗透对照组);iii. 用50 mM D-葡萄糖处理的细胞(高糖组);iv. 用50 mM D-葡萄糖+纳米氧化铈处理的细胞。测量细胞活力、ROS形成、LPO和GSH,并进行统计学分析。
高糖(50 mM)处理导致HepG2细胞显著死亡,并增加氧化应激标志物。有趣的是,50 mM浓度的纳米氧化铈显著降低了高糖诱导的细胞毒性、ROS形成和LPO。该浓度的纳米氧化铈增加了HepG2细胞中的GSH含量(P<0.05)。
纳米氧化铈颗粒的抗氧化特性使其成为减轻不同器官高血糖氧化损伤的有吸引力的候选物。