生姜对化学致癌物导致的肝细胞癌变有保护作用

 

生姜成分抑制了大鼠化学肝癌模型中二乙基亚硝胺诱导的癌前恶变表型的发展

Ginger ingredients inhibit the development of diethylnitrosoamine induced premalignant phenotype in rat chemical hepatocarcinogenesis model.

 

翻译:蓝山

 

由沙特阿拉伯国王大学药学院College of Pharmacy, King Saud University进行的研究,发现生姜对化学致癌物导致的肝细胞癌变有保护作用。

 

为了研究生姜提取物对乙基亚硝基胺(DEN)引发,并被四氯化碳(CCl(4))促进肝癌的可能的抗肿瘤活性。将60只雄性Wistar白化大鼠分为4组,每组15只。第1组大鼠(对照组)接受单一腹腔注射生理盐水。第2组的动物在饮用水中加入生姜(50毫克/公斤/),持续8周。第3组大鼠(DEN)注射单次DEN (200 mg/kg, i.p) 2周后,通过灌胃1(2 mL/kg i.g),按1:1稀释玉米油。第4(DEN -ginger)的动物在接受了第三组一样的致癌诱导方案,

另加肝癌发生前的2周内,在饮用水中 加入生姜(50 mg/kg/),并在整个实验期间继续进行。

 

 

在雄性Wistar大鼠中,由乙基亚硝胺启动和四氯化碳促进的肝脏癌变表现血清升高的肝脏肿瘤标志物α-甲胎蛋白和癌胚抗癌水平。此外,肝组织生长因子血管内皮生长因子、碱性成纤维细胞生长因子和羟脯氨酸含量的显著增加进一步证实了肝癌的发生。还观察到内皮抑素和金属蛋白的显著减少。

 

在肝癌发生前2周长期给予生姜提取物及整个实验期间给予生姜均可防止金属硫蛋白和内皮抑素的肝含量降低,以及致癌物诱导的生长因子的增加。此外,生姜提取物使血清肝脏肿瘤标志物正常。肝脏组织病理学检查也与生化观察有关。这些发现表明,生姜提取物对乙基亚硝基胺(DEN)引发,并被四氯化碳(CCl(4))促进大鼠肝细胞癌变的保护作用

 

 

参考文献:

 

Ginger ingredients inhibit the development of diethylnitrosoamine induced premalignant phenotype in rat chemical hepatocarcinogenesis model.

Mansour MA1, Bekheet SA, Al-Rejaie SS, Al-Shabanah OA, Al-Howiriny TA, Al-Rikabi AC, Abdo AA.

Author information

1

Department of Pharmacology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia. mansour1960us@hotmail.com

Abstract

To investigate the possible antitumor activity of ginger extract against hepatic carcinogenesis initiated by diethylnitrosoamines (DEN) and promoted by carbon tetrachloride (CCl(4) ). A total of 60 male Wistar albino rats were divided into four groups with 15 animals in each group. Rats in group 1 (control group) received a single intraperitoneal (i.p.) injection of normal saline. Animals in group 2 were given ginger (50 mg/kg/day) in drinking water for 8 weeks. Rats in group 3 (DEN group) were injected with a single dose of DEN (200 mg/kg, i.p.), 2 weeks later received a single dose of CCl(4) (2 mL/kg i.g) by gavage as 1:1 dilution in corn oil. Animals in group 4 (DEN-ginger group) received the same carcinogenesis induction protocol as in group 3 plus ginger (50 mg/kg/day) in drinking water for 2 weeks before induction of hepatocarcinogenesis and continued throughout the experimental period. DEN-initiated and CCl(4) -promoted hepatocarcinogenesis in male Wistar rats was manifested biochemically by elevation of serum hepatic tumor markers tested; α-fetoprotein and carcinoembryonic antigen. In addition, hepatocarcinogenesis was further confirmed by a significant increase in hepatic tissue growth factors; vascular endothelial growth factor, basic fibroblast growth factor, and hydroxyproline content. A marked decrease in endostatin and metallothonein were also observed. Long-term ginger extract administration 2 weeks before induction of hepatocarcinogenesis and throughout the experimental period prevented the decrease of the hepatic content of metallothionein and endostatin and the increase in the growth factors induced by the carcinogen. Moreover, ginger extract normalize serum hepatic tumor markers. Histopathological examination of liver tissue also correlated with the biochemical observations. These findings suggest a protective effect of ginger extract against premalignant stages of liver cancer in the DEN-initiated and CCl(4) -promoted hepatocarcinogenesis model in rats.

https://www.ncbi.nlm.nih.gov/pubmed/?term=20872761