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曼氏血吸虫感染小鼠肝脏中P53和CD68的表达及水飞蓟素的保护作用

Expressions of P53 and CD68 in mouse liver with Schistosoma mansoni infection and the protective role of silymarin.

作者信息

Tousson Ehab, Beltagy Doha M, Gazia Maha Abo, Al-Behbehani Bahija

机构信息

Department of Zoology, Tanta University, Egypt.

出版信息

Toxicol Ind Health. 2013 Sep;29(8):761-70. doi: 10.1177/0748233712442733. Epub 2012 Apr 16.

Abstract

Schistosomiasis is one of the major human parasitic diseases in many developing countries and is one of the causes of morbidity and mortality in the human population. The present work has been planned to study the histopathological and immunohistochemical expression of P53 and CD68 in mouse liver tissues experimentally infected with Schistosoma mansoni, in addition to the ameliorating role of silymarin. A total of 50 adult male mice were divided into 5 groups (10 animals each). Groups 1 and 2 were the control and silymarin groups, respectively, while group 3 was the infected group in which the mice were infected with S. mansoni live cercariae for 6 weeks. Groups 4 and 5 were the cotreated and posttreated groups, respectively, in which mice were infected with cercariae of S. mansoni and treated with silymarin during and after Schistosoma infection, respectively. The major histopathological lesions were variable numbers of perioval granulomas, diffuse infiltration of inflammatory cells, mainly eosinophils and small mononuclear cells, and fibrosis of portal areas and interlobular septa. Treatment with silymarin led to a significant reduction in granuloma area in all treated infected mice compared with nontreated infected mice. Immunohistochemical observations of the liver tissues showed a significant increase in the apoptotic proteins P53 and CD68 after the infection with the cercariae of Schistosoma, compared with the control group. The expression of the cytoplasmic P53 and CD68 was very low in the control liver sections. A significant decrease in the expression of the cytoplasmic P53 and CD68 was observed after silymarin treatment.

摘要

血吸虫病是许多发展中国家主要的人类寄生虫病之一,也是导致人类发病和死亡的原因之一。本研究旨在探讨在实验性感染曼氏血吸虫的小鼠肝脏组织中P53和CD68的组织病理学及免疫组化表达,以及水飞蓟宾的改善作用。总共50只成年雄性小鼠被分为5组(每组10只动物)。第1组和第2组分别为对照组和水飞蓟宾组,而第3组为感染组,小鼠感染曼氏血吸虫活尾蚴6周。第4组和第5组分别为联合治疗组和治疗后组,小鼠分别在感染曼氏血吸虫尾蚴期间和之后用水飞蓟宾进行治疗。主要的组织病理学病变为数量不等的卵周肉芽肿、炎症细胞弥漫浸润,主要为嗜酸性粒细胞和小单核细胞,以及门管区和小叶间隔纤维化。与未治疗的感染小鼠相比,水飞蓟宾治疗使所有治疗的感染小鼠的肉芽肿面积显著减小。肝脏组织的免疫组化观察显示,与对照组相比,感染曼氏血吸虫尾蚴后凋亡蛋白P53和CD68显著增加。在对照肝脏切片中,细胞质P53和CD68的表达非常低。水飞蓟宾治疗后,细胞质P53和CD68的表达显著降低。

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