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首页> 外文期刊>Journal of biochemical and molecular toxicology >Protective effect of arjunolic acid against arsenic-induced oxidative stress in mouse brain.
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Protective effect of arjunolic acid against arsenic-induced oxidative stress in mouse brain.

机译：阿魏酸对小鼠脑中砷诱导的氧化应激的保护作用。

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摘要

Arsenic, a notoriously poisonous metalloid, is ubiquitous in the environment, and it affects nearly all organ systems of animals including humans. The present study was designed to investigate the preventive role of a triterpenoid saponin, arjunolic acid against arsenic-induced oxidative damage in murine brain. Sodium arsenite was selected as a source of arsenic for this study. The free-radical-scavenging activity and the in vivo antioxidant power of arjunolic acid were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly decreased the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase, the level of cellular metabolites, reduced glutathione, total thiols and increased the level of oxidized glutathione. In addition, it enhanced the levels of lipid peroxidation end products and protein carbonyl content. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration almost normalized above indices. Histological findings due to arsenic intoxication and arjunolic acid treatment supported the other biochemical changes in murine brains. Results of 2,2-diphenyl-1-picryl hydrazyl radical scavenging and ferric reducing/antioxidant power assays clearly showed the in vitro radical scavenging as well as the in vivo antioxidant power of arjunolic acid, respectively. The effect of a well-established antioxidant, vitamin C, has been included in the study as a positive control. Combining all, results suggest that arjunolic acid possessed the ability to ameliorate arsenic-induced oxidative insult in murine brain and is probably due to its antioxidant activity.
机译：砷是一种臭名昭著的有毒准金属，在环境中无处不在，它几乎影响着动物的所有器官系统，包括人类。本研究旨在研究三萜皂苷，芥酸对砷诱导的鼠脑氧化损伤的预防作用。本研究选择了亚砷酸钠作为砷的来源。分别从其2，2-二苯基-1-苦基肼基自由基清除能力和三价铁还原/抗氧化能力测定中确定了芳酸的自由基清除活性和体内抗氧化能力。口服亚砷酸钠剂量为10 mg / kg体重持续2天，可显着降低抗氧化酶，超氧化物歧化酶，过氧化氢酶，谷胱甘肽S-转移酶，谷胱甘肽还原酶和谷胱甘肽过氧化物酶的活性，降低了细胞代谢产物的水平谷胱甘肽，总硫醇和增加氧化型谷胱甘肽的水平。此外，它提高了脂质过氧化终产物的水平和蛋白质羰基含量。在施用砷之前，以20 mg / kg体重的剂量用正酸进行治疗4天，几乎使上述指标恢复正常。砷中毒和阿魏酸处理引起的组织学发现支持了鼠脑中的其他生化变化。 2，2-二苯基-1-吡啶基肼基自由基清除和三价铁还原/抗氧化能力测定的结果分别清楚地表明，体外清除自由基和体内抗氧化能力均是阿魏酸。成熟的抗氧化剂维生素C的作用已作为阳性对照纳入研究。综上所述，结果表明，壬酸具有改善砷诱导的鼠脑氧化损伤的能力，这可能是由于其抗氧化活性所致。

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