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双(4-甲基苯甲酰)二硒醚对 CCl(4)诱导的小鼠氧化损伤的保护作用。

Hepatoprotective effect of bis(4-methylbenzoyl) diselenide against CCl(4)-induced oxidative damage in mice.

机构信息

Laboratório de Avaliações Farmacológicas e Toxicológicas Aplicadas às Moléculas Bioativas, LaftamBio Pampa, Universidade Federal do Pampa, CEP 97650-000, Itaqui, RS, Brazil.

出版信息

Cell Biochem Funct. 2013 Mar;31(2):152-8. doi: 10.1002/cbf.2869. Epub 2012 Sep 7.

DOI:10.1002/cbf.2869
PMID:22961633
Abstract

From a pharmacological point of view, organoseleniums are compounds with important and interesting antioxidant and biological activities. The aim of this study was to evaluate the hepatoprotective effect of bis(4-methylbenzoyl) diselenide (BMD) against carbon tetrachloride (CCl4 )-induced oxidative damage in mice. The animals received BMD (25 mg/kg p.o., for 3 days), and after 1 day, CCl4 (1 mg/kg body weight) was administered by intraperitoneal route. One day after the CCl4 exposure, the animals were euthanized for biochemical and histological analysis. Treatment with BMD (25 mg/kg p.o.) protected against aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transferase and lactate dehydrogenase activity increases induced by CCl4 plasma exposure. Treatment with BMD (25 mg/kg) protected against increases in thiobarbituric reactive species and decreasing non-protein thiols and ascorbic acid levels in liver of mice. Catalase and superoxide dismutase activity inhibition in the liver caused by CCl4 were protected by treatment with BMD (25 mg/kg). Glutathione S-transferase activity was inhibited by CCl4 and remained unaltered even after treatment with BMD. Sections of liver from CCl4 -exposed mice presented an intense infiltration of inflammatory cells and loss of the cellular architecture. BMD (25 mg/kg) attenuated CCl4 -induced hepatic histological alterations. The results demonstrated the hepatoprotective effects of BMD in the mouse liver, possibly by modulating the antioxidant status.

摘要

从药理学角度来看,有机硒化合物具有重要且有趣的抗氧化和生物活性。本研究旨在评估双(4-甲基苯甲酰)二硒醚(BMD)对四氯化碳(CCl4)诱导的小鼠氧化损伤的肝保护作用。动物接受 BMD(25mg/kg,po,连续 3 天)治疗,1 天后,通过腹腔途径给予 CCl4(1mg/kg 体重)。在 CCl4 暴露 1 天后,处死动物进行生化和组织学分析。BMD(25mg/kg,po)治疗可预防 CCl4 引起的血浆天门冬氨酸氨基转移酶、丙氨酸氨基转移酶、碱性磷酸酶、γ-谷氨酰转移酶和乳酸脱氢酶活性升高。BMD(25mg/kg)治疗可预防 CCl4 引起的肝组织中硫代巴比妥酸反应性物质增加和非蛋白巯基及抗坏血酸水平降低。BMD(25mg/kg)可预防 CCl4 引起的肝组织中过氧化氢酶和超氧化物歧化酶活性抑制。CCl4 可抑制谷胱甘肽 S-转移酶活性,即使在用 BMD 治疗后,其活性仍未改变。CCl4 暴露的小鼠肝组织切片显示炎症细胞浸润强烈,细胞结构丧失。BMD(25mg/kg)可减轻 CCl4 引起的肝组织学改变。结果表明,BMD 对小鼠肝脏具有肝保护作用,可能通过调节抗氧化状态。

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