血管生成抑制在非酒精性脂肪性肝病大鼠模型中的可能作用

D. M. A. G. Rezk, Mohammed E. Sarhan, hanaa ahmed abdel moniem, A. Abbas, M. E. Salama
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引用次数: 1

摘要

目的:观察NAFLD大鼠血管生成的情况,探讨抗血管生成治疗(索拉非尼)对NAFLD进展的保护作用。方法:将45只白化病大鼠(200 ~ 300 g)分为3组,每组15只:第一组:对照组,饲喂普通饲料。第二组:大鼠给予高脂肪、高果糖饮食(HFD、HFr)和DEN(每周2次,共8周,ip)。III组:大鼠口服HFD、HFr + DEN +索拉非尼8周。进行生化、组织病理学及免疫组织病理学检查。结果:高脂、高果糖饮食加DEN导致血清胆固醇、TG、LDL、AST、ALT显著升高,HDL、白蛋白水平显著降低,肝脏GSH显著降低,组织病理学检查显示,未经DEN治疗的大鼠肝脏出现严重的脂肪浸润(3级)。未经治疗的NAFLD大鼠肝脏免疫组化检查显示对VEGF、α- SMA、CD31和Caspase3抗体有较强的染色反应。口服索拉非尼可缓解上述症状。
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Possible role of angiogenesis suppression in rats model of non alcoholic fatty liver disease
Objective:to evaluate development of angiogenesis in rats of NAFLD and to determine the protective effects of antiangiogenic therapy (sorafenib) in preventing the progression of NAFLD. Methods: 45 Albino rats (200-300 g) were divided into 3 groups (15 rats for each): Group I: Control group fed on an ordinary diet. Group II: rats received high fat, high fructose diet (HFD,HFr) with DEN ( twice weekly for 8 weeks, ip). Group III: rats received HFD, HFr + DEN + sorafenib orally for 8 weeks. Biochemical, histopathologial, and immunohistopathological examination were studied. Results: high fat, high fructose diet with DEN resulted in a significant elevation in the serum cholesterol, TG, LDL, and AST, and ALT, significantly lower levels of HDL and Albumin together with a significant decrease in hepatic GSH, Histopathological examination revealed that liver of untreated rats showed severe fatty infilteration (grade3). Immunohistochemical examination of liver of untreated NAFLD rats showed strong staining reactions against VEGF, α- SMA, CD31, and Caspase3 antibodies. Oral administration of sorafenib alleviated all these parameters.
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