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诃子可保护小鼠心脏免受氟化钠诱导的氧化应激损伤。

Terminalia arjuna protects mouse hearts against sodium fluoride-induced oxidative stress.

作者信息

Sinha Mahua, Manna Prasenjit, Sil Parames C

机构信息

Department of Chemistry, Bose Institute, Kolkata, India.

出版信息

J Med Food. 2008 Dec;11(4):733-40. doi: 10.1089/jmf.2007.0130.

Abstract

Fluoride is a ubiquitous environmental pollutant. In the current study we have investigated the antioxidative properties of an ethanol extract of the bark of Terminalia arjuna (T. arjuna ethanol extract [TAEE]) against sodium fluoride (NaF)-induced oxidative stress in murine heart. Experimental mice were divided into four groups. The first group served as the normal control. The second group received NaF at a dose of 600 ppm through drinking water for 1 week and served as the toxin control. The third group was exposed to TAEE (at a dose of 50 mg/kg of body weight for 1 week) prior to NaF intoxication, and the last group was treated with vitamin C at a dose of 100 mg/kg body weight for 1 week prior to NaF intoxication and served as the positive control in the study. The activities of various antioxidant enzymes (superoxide dismutase, catalase, and glutathione S-transferase), levels of cellular metabolites, reduced glutathione, and oxidized glutathione, levels of lipid peroxidation end products, and protein carbonyl contents were determined in the cardiac tissues of all the experimental animals. NaF intoxication significantly altered all the indices related to the prooxidant-antioxidant status of the heart; treatment with the active constituents prior to NaF administration, however, prevented these alterations. In addition, the ferric reducing/antioxidant power assay revealed that TAEE enhanced the cardiac intracellular antioxidant activity. Histological studies also demonstrated a cardioprotective action of TAEE. The combined results suggest that TAEE protects murine hearts from NaF-induced oxidative stress, probably via its antioxidant properties.

摘要

氟化物是一种普遍存在的环境污染物。在本研究中,我们调查了诃子树皮乙醇提取物(TAEE)对氟化钠(NaF)诱导的小鼠心脏氧化应激的抗氧化特性。实验小鼠分为四组。第一组作为正常对照组。第二组通过饮用水给予600 ppm的NaF,持续1周,作为毒素对照组。第三组在NaF中毒前接受TAEE(剂量为50 mg/kg体重,持续1周),最后一组在NaF中毒前以100 mg/kg体重的剂量给予维生素C,持续1周,作为本研究的阳性对照组。测定了所有实验动物心脏组织中各种抗氧化酶(超氧化物歧化酶、过氧化氢酶和谷胱甘肽S-转移酶)的活性、细胞代谢物、还原型谷胱甘肽和氧化型谷胱甘肽的水平、脂质过氧化终产物的水平以及蛋白质羰基含量。NaF中毒显著改变了所有与心脏促氧化剂-抗氧化剂状态相关的指标;然而,在给予NaF之前用活性成分进行治疗可预防这些改变。此外,铁还原/抗氧化能力测定表明TAEE增强了心脏细胞内的抗氧化活性。组织学研究也证明了TAEE的心脏保护作用。综合结果表明,TAEE可能通过其抗氧化特性保护小鼠心脏免受NaF诱导的氧化应激。

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