首页> 外文期刊>Journal of biochemical and molecular toxicology >Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver.
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Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver.

机译:咖啡酸苯乙酯(CAPE)对糖尿病大鼠肝脏脂质过氧化和抗氧化酶的保护作用。

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The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver of streptozotocin (STZ)-induced diabetic rats. Twenty-seven rats were randomly divided into three groups: group I, control non-diabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 8); group III, STZ-induced, CAPE-treated diabetic rats (n = 10), which were intraperitoneally injected with CAPE (10 渭M kg(-1) day(-1)) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH-Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (p < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH-Px in the untreated diabetic group were higher than that in the control group (p < 0.0001). The activities of SOD and GSH-Px in the CAPE-treated diabetic group were higher than that in the control group (respectively, p < 0.0001, p < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE-treated diabetic and control groups. Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (p < 0.0001). There were no significant differences in the activity of GSH-Px between the rats of untreated diabetic and CAPE-treated groups. It is likely that STZ-induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ-induced diabetic damage. CAPE can reduce LPO caused by STZ-induced diabetes. (c) 2004 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:234-238, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20028.
机译:这项研究的目的是研究咖啡酸苯乙酯(CAPE)对脂质过氧化(LPO)的影响以及抗氧化剂酶的活性,例如超氧化物歧化酶(SOD),过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px) )在链脲佐菌素(STZ)诱导的糖尿病大鼠的肝脏中。二十七只大鼠随机分为三组:第一组,对照组非糖尿病大鼠(n = 9);第二组。 II组,STZ诱导的未治疗的糖尿病大鼠(n = 8);第III组,STZ诱导的,CAPE治疗的糖尿病大鼠(n = 10),其在3天后腹膜内注射CAPE(10μMkg(-1)day(-1)),然后进行STZ治疗。 CAPE治疗8周后切除肝脏,分析各组肝组织中丙二醛(MDA)的水平以及SOD,CAT和GSH-Px的活性。在未治疗的糖尿病大鼠中,与对照组相比,肝组织中的MDA显着增加(p <0.0001)。但是,CAPE将MDA水平降低至对照水平。未经治疗的糖尿病组的SOD,CAT和GSH-Px活性高于对照组(p <0.0001)。 CAPE治疗的糖尿病组的SOD和GSH-Px活性高于对照组(分别为p <0.0001,p <0.035)。在CAPE治疗的糖尿病组和对照组之间,CAT的活性没有显着差异。与未治疗的糖尿病组相比,CAPE治疗的糖尿病组大鼠的SOD和CAT活性降低(p <0.0001)。未治疗的糖尿病组和CAPE治疗组的大鼠之间的GSH-Px活性没有显着差异。 STZ诱发的糖尿病很可能引起肝损害。另外,LPO可能是STZ诱导的糖尿病损害的分子机制之一。 CAPE可以减少STZ诱导的糖尿病引起的LPO。 (c)2004 Wiley Periodicals,Inc. J Biochem Mol Toxicol 18:234-238,2004;在线发布于Wiley InterScience(www.interscience.wiley.com)。 DOI 10.1002 / jbt.20028。

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