乳铁蛋白对成年雄性白化大鼠实验性肝纤维化影响的组织学评估

Shimaa M. Badr, Hoda Ibrahim, M. Elkelany
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引用次数: 0

摘要

背景:四氯化碳(CCl4)诱导的肝纤维化是一种成熟的肝毒性模型。乳铁蛋白(LF)是一种铁结合糖蛋白,具有抗炎和抗氧化作用。研究目的本研究采用各种生化和组织学技术,证明乳铁蛋白对 CCL4 诱导的成年雄性白化大鼠肝纤维化的改善作用。材料与方法:本研究将 40 只成年雄性白化大鼠随机分为 4 组:I 组为对照组;II 组口服乳铁蛋白(100 毫克/千克/天),连续 5 周;III 组腹腔注射 CCL4(1 毫升/千克/每周一次,连续 5 周)以诱导肝纤维化;IV 组同时口服乳铁蛋白和 CCL4,剂量和方式分别与 II 组和 III 组相同。对肝脏标本进行不同的生化、组织学和免疫组化技术处理。还进行了形态计量学和统计学研究。结果光镜和电子显微镜检查显示,CCL4 组肝脏结构紊乱。用马森氏三色染色法检测胶原纤维的平均面积百分比明显增加,沿肝窦的αSMA和CD133免疫阳性反应也被观察到。第四组服用乳铁蛋白后,所有先前的结果和氧化应激生物标志物均有所改善。结论乳铁蛋白可改善肝纤维化。运行
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Histological Evaluation of the Effect of Lactoferrin on Experimentally Induced Liver Fibrosis in Adult Male Albino Rat
Background: Carbon tetrachloride (CCl4)-induced liver fibrosis is a well-established model of hepatotoxicity. Lactoferrin (LF) is an iron-binding glycoprotein that has anti-inflammatory and antioxidant effects. Aim of the study: This study was made to demonstrate the ameliorating effect of lactoferrin versus CCL4 induced liver fibrosis in adult male albino rat using various biochemical and histological techniques. Materials & Methods: This study involved forty adult male albino rats that were randomly divided into 4 groups: group I represented the control group, group II received LF (100mg/kg/day) orally for 5 weeks , group III was intraperitoneally injected with CCL4 (1ml/kg/once a week, for five weeks) for induction of liver fibrosis, and group IV received LF and CCL4 concomitantly in the same dose and manner as groups II & III respectively. The liver specimens were processed for different biochemical, histological and immunohistochemical techniques. Morphometrical and statistical studies were also performed. Results: CCL4 group showed disorganization of liver architecture that was evidenced by light & electron microscopic examination. A significant increase of the mean area percentage of collagen fibers by Masson’s Trichrome, immunopositive reaction of αSMA and CD133 along the sinusoids were also observed. Lactoferrin administration in group IV showed improvement of all the previous results and oxidative stress biomarkers. Conclusion: Liver fibrosis could be ameliorated by lactoferrin. Running
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