CASPASE-3 and FAS-L expression and their roles as signal transduction in hepatocellular carcinoma

S. Hamdy, Saad M. El-Gendy, S. Atrees
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引用次数: 3

Abstract

Hepatocellular carcinoma (HCC) is a common malignant affecting approximately-one million of people around the world every year. This study aimed to early recognition of the carcinogenic effect of N-nitrosodiethlyamine (NDEA) on hepatocytes and expression of Fas-L and Caspase-3. The study was done using tissue homogenate of 60 male albino rats divided into 2 groups: group 1,control group (30 rats) and Group 2, -N-nitrosodiethylamine (NDEA) treated group (NDEA, in a single dose 200 mg/Kg wt and; Carbon tetrachloride (CCL4), twice per week 3 ml/Kg wt) (30 rats). 10 rats from each control and treated group were sacrificed at the 1st, 2n , and 3rd months of the treatment for evaluation (1) of glutathione s transferase(GST), glutathione peroxidase (GPx), glutathione reductase (GRase), glutathione reduced form (GSH), superoxide dismutase (SOD) levels, (2) studying expression of Fas-L and Caspase-3 and (3) for histopathological examination. The results revealed that the treated group antioxidant enzymes levels (Glutathione family and SOD) showed a significant decrease with gradual rates through the three months of the treated compared to the control group, whereas the GRase level was significantly increased compared to the control group. Caspase-3 and Fas-L in liver tissue homogenate in the treated group was significantly decreased in comparison with the control group. The histopathological results showed pronounced changes with evident fatty degeneration (steatosis), marked microvascular steatosis with malignant hepatocytes amounting grade 1. Finally, study can conclude that investigation of liver tissue markers induced by the chemical carcinogen NDEA at different stages of the development of cancer could help in getting more information about the development of HCC and more investigated studies on Caspase-3 and Fas-L, could be a promising way for the treatment of HCC.
CASPASE-3和FAS-L在肝细胞癌中的表达及其信号转导作用
肝细胞癌(HCC)是一种常见的恶性肿瘤,每年影响全球约100万人。本研究旨在早期发现n -亚硝基二乙胺(NDEA)对肝细胞及Fas-L和Caspase-3表达的致癌作用。选用60只雄性白化大鼠组织匀浆,分为2组:1组为对照组(30只),2组为-n -亚硝基二乙胺(NDEA)处理组(NDEA),单次给药200 mg/Kg wt和;四氯化碳(CCL4),每周2次3ml /Kg wt)(30只大鼠)。各组分别于治疗后1、2、3个月处死10只大鼠,测定(1)谷胱甘肽转移酶(GST)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GRase)、谷胱甘肽还原型(GSH)、超氧化物歧化酶(SOD)水平,(2)Fas-L和Caspase-3的表达,(3)进行组织病理学检查。结果显示,与对照组相比,治疗组抗氧化酶水平(谷胱甘肽家族和超氧化物歧化酶)在三个月内呈逐渐下降趋势,而与对照组相比,GRase水平显著升高。治疗组肝组织匀浆中Caspase-3、Fas-L含量较对照组显著降低。组织病理学结果显示明显的脂肪变性(脂肪变性),微血管脂肪变性明显,恶性肝细胞达1级。最后,研究可以得出结论,研究化学致癌物NDEA在不同癌症发展阶段诱导的肝组织标志物有助于获得更多关于HCC发展的信息,对Caspase-3和Fas-L的深入研究可能是HCC治疗的一种有希望的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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