缓激肽增强因子、丁基羟基甲苯和奥替praz对黄曲霉中毒雌性大鼠淋巴器官生化和组织学结构的改善作用

S. Mahgoub, A. Nassar, H. Omar, Amany M. A. Osman
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摘要

黄曲霉毒素(AFs)是由曲霉、青霉和镰刀菌属产生的化学次生代谢物。由于抑制大分子合成,对人类和动物的健康有不良影响。本研究观察了雌性大鼠暴露于黄曲霉毒素B1 (AFB1)一个月后淋巴滤泡的病理生化变化,以及眼镜蛇蛇毒中分离的缓动肽增强因子(BPF)、丁基羟基甲苯(BHT)和奥替praz (OPZ)对这些变化的改善作用。黄曲霉中毒引起脂肪过氧化(LPO)和一氧化氮(NO)显著升高,总硫醇、谷胱甘肽(GSH)水平显著降低,谷胱甘肽过氧化物酶(GPx)和谷胱甘肽s转移酶(GST)活性显著降低。此外,AFB1引起Safaa A. Mahgoub等人27 http://www.aun.edu.eg E-mail: president@aun.edu.eg淋巴滤泡的组织病理学改变,表现为淋巴样细胞的耗损。用BPF、BHT或OPZ治疗黄曲霉中毒大鼠,可改善氧化应激标志物,改善淋巴滤泡的组织学结构,表现为淋巴样细胞群增加,肥大细胞和胶原束存在。结论BPF、BHT或OPZ对黄曲霉中毒的改善作用以BPF为主。
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Ameliorative effects of bradykinin potentiating factor, butylated hydroxy toluene and oltipraz on biochemical and histological structure of lymphoid organs in aflatoxicated female rats
Aflatoxins (AFs) are chemically secondary metabolites produced by Aspergillus, Penicillium and Fusarium genera. It has adverse effects on humans and animals health due to inhibition of macromolecule synthesis. The current research investigate the pathological and biochemical changes in lymph follicles of female rats exposed to aflatoxin B1 (AFB1) for one month and the efficacy of isolated bradykinin potentiating factor (BPF) from cobra snake venom, butylated hydroxy toluene (BHT) and oltipraz (OPZ) to ameliorate those changes. Aflatoxicosis cause significant increase of lipid peroxidation (LPO) and nitric oxide (NO) in addition to significant decrease in the level of total thiols, glutathione (GSH) and the activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Moreover, AFB1 caused Safaa A. Mahgoub et al. 27 http://www.aun.edu.eg E-mail: president@aun.edu.eg histopathological changes in lymph follicles represented by depletion of the lymphoid cells. Treatment of aflatoxicosed rats with BPF, BHT or OPZ resulting in amelioration of the oxidative stress markers and improvement in the histological structure of lymph follicles represented by increase of lymphoid cell population with presence of mast cells and collagen bundle. In conclusion BPF, BHT or OPZ ameliorate the aflatoxicosis with priority for the BPF.
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