Alzaidi Mohammed Azeez, Arab Hossein Ali, Amanpour Saeid, Shirkoohi Reza, Muhammadnejad Samad, Sasani Farhang
Department of Pharmacology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Cancer Biology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
J Gastrointest Cancer. 2018 Jun;49(2):172-180. doi: 10.1007/s12029-017-0050-7.
Some epidemiological studies have shown an association between opium consumption and the incidence of gastrointestinal (GI) cancer. The present study was designed to investigate the effects of opium on the initiation of GI cancer in rats.
Forty-five rats were randomly divided into three groups; each received different treatment for 40 weeks. The rats in group 1 received purified water, while animals in group 2 were treated with 5 mg/kg diethylnitrosamine (DEN) orally for 8 weeks and continued with purified water by the end of the experiment. The third experimental group received 300 mg/kg opium for 16 weeks and then continued with 50 mg/kg phenobarbital by the end of the 40th week. The growth of tumors in the treated groups was assessed by histological changes and the up/down expression of p53, cdkn1, cdk2, e-cdh, and n-cdh genes in different parts of GI tract.
Histological examinations revealed that DEN was able to induce the growth of tumor in GI tract as shown by active mitotic figure in different regions of GI system and hyperplasia of hepatocytes associated with infiltration of inflammatory cells, intestinal villous hypertrophy, and colorectal adenoma. There was also significant (p < 0.05) overexpression of p53, cdk2, and n-Cdh genes in different parts of digestive system in DEN-treated group. However, these pathological changes and the degradation of gene expression were not observed in the opium-treated group.
The results of this study suggest that the opium does not promote the initiation of cancer in GI tract.
一些流行病学研究表明鸦片消费与胃肠道（GI）癌的发病率之间存在关联。本研究旨在调查鸦片对大鼠胃肠道癌起始的影响。
45只大鼠随机分为三组；每组接受不同处理40周。第1组大鼠饮用纯净水，而第2组动物口服5mg/kg二乙基亚硝胺（DEN），持续8周，实验结束时继续饮用纯净水。第三实验组在16周内接受300mg/kg鸦片，然后在第40周结束时继续接受50mg/kg苯巴比妥。通过组织学变化以及胃肠道不同部位p53、cdkn1、cdk2、e-cdh和n-cdh基因的上调/下调表达来评估处理组中肿瘤的生长情况。
组织学检查显示，DEN能够诱导胃肠道肿瘤生长，表现为胃肠道系统不同区域有活跃的有丝分裂象，肝细胞增生并伴有炎性细胞浸润、肠绒毛肥大和结肠直肠腺瘤。在DEN处理组的消化系统不同部位，p53、cdk2和n-Cdh基因也有显著（p<0.05）的过表达。然而，在鸦片处理组中未观察到这些病理变化和基因表达的降解。
本研究结果表明，鸦片不会促进胃肠道癌的起始。
