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杏和β-胡萝卜素对甲氨蝶呤诱导的大鼠肠道氧化损伤的强大保护作用。

Potent protective effect of apricot and beta-carotene on methotrexate-induced intestinal oxidative damage in rats.

作者信息

Vardi Nigar, Parlakpinar Hakan, Ozturk Feral, Ates Burhan, Gul Mehmet, Cetin Asli, Erdogan Ali, Otlu Ali

机构信息

Department of Embryology and Histology, Inonu University, 44280 Malatya, Turkey.

出版信息

Food Chem Toxicol. 2008 Sep;46(9):3015-22. doi: 10.1016/j.fct.2008.05.039. Epub 2008 Jun 14.

Abstract

Several studies have well confirmed the contribution of oxidative stress in the pathogenesis of methotrexate (MTX)-induced damage in the small intestine. Many agents have been tried experimentally to reduce or inhibit the oxidative stress. To our knowledge, there is no study about apricot consumption on the MTX-induced damage in the small intestine. The aim of this study was to determine the possible protective effects of apricot and beta-carotene on MTX-induced intestinal damage in rats. The rats were randomly divided into seven groups as follows; I-control group; II-apricot group; III-beta-carotene group; IV-MTX group; V-apricot+MTX group; VI-beta-carotene+MTX group and VII-apricot+beta-carotene+MTX group. In the MTX group; fusion and shortening in the villus, epithelial desquamation, crypt loss, inflammatory cell infiltration in the lamina propria, goblet cell depletion and microvillar damage were observed in the small intestine. Parallel to histological results, malondialdehyde (MDA) content and myeloperoxidase (MPO) activity were found to be increased, whereas superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP-x) activities and glutathione (GSH) content were decreased in the MTX group. However, single or combined application of apricot and beta-carotene ameliorated all of these hazardous effects in antioxidant system in MTX-treated groups. In conclusion, our results demonstrate that apricot and/or beta-carotene treatment may protect the impairment of oxidative stress and ameliorate MTX-induced intestine damage at biochemical and histological levels.

摘要

多项研究已充分证实氧化应激在甲氨蝶呤(MTX)诱导的小肠损伤发病机制中的作用。人们已通过实验尝试了多种药物来减轻或抑制氧化应激。据我们所知,尚无关于食用杏子对MTX诱导的小肠损伤影响的研究。本研究旨在确定杏子和β-胡萝卜素对MTX诱导的大鼠肠道损伤可能具有的保护作用。大鼠被随机分为以下七组:I-对照组;II-杏子组;III-β-胡萝卜素组;IV-MTX组;V-杏子+MTX组;VI-β-胡萝卜素+MTX组和VII-杏子+β-胡萝卜素+MTX组。在MTX组中,观察到小肠绒毛融合、缩短,上皮细胞脱落,隐窝消失,固有层炎性细胞浸润,杯状细胞减少以及微绒毛损伤。与组织学结果一致,MTX组丙二醛(MDA)含量和髓过氧化物酶(MPO)活性升高,而超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GP-x)活性以及谷胱甘肽(GSH)含量降低。然而,杏子和β-胡萝卜素单独或联合应用改善了MTX治疗组抗氧化系统中的所有这些有害影响。总之,我们的结果表明,杏子和/或β-胡萝卜素治疗可能在生化和组织学水平上保护氧化应激损伤并改善MTX诱导的肠道损伤。

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