Selvendiran Karuppaiyah, Banu Syed Mumtaz, Sakthisekaran Dhanapal
Department of Medical Biochemistry, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600 113, India.
Clin Chim Acta. 2004 Dec;350(1-2):73-8. doi: 10.1016/j.cccn.2004.07.004.
The statistics on lung cancer necessitates the urge to develop new methods to control this most deadly form of cancer. Chemoprevention is one of these new approaches. Carcinogens from cigarette smoke form the link between nicotine addiction and lung cancer. At the same time, it has become increasingly clear that dietary and genetically determined factors play an important role in modulating the individual susceptibility and are linked to the chemoprevention approach. In this study, the ability of piperine to prevent lung carcinogenesis in mice was characterized and its effects on cell proliferation and protein damage biomarkers were determined.
Thirty Swiss albino mice were divided into five groups of six animals each. Animals in group I received corn oil orally and served as control. Group II were administered with 50 mg/kg b.wt. of benzo(a)pyrene (B(a)P) twice a week for 4 consecutive weeks to induce lung cancer by the end of 16th week. Group III received 50 mg/kg b.wt. piperine on alternate days for 16 weeks immediately after the first dose of carcinogen. Group IV also received piperine as in group III but from the sixth week of B(a)P induction till the end of the experiment. Group V animals constituted the drug control and received piperine alone.
Administration of piperine significantly decreased the levels of lipid peroxidation, protein carbonyls, nucleic acid content and polyamine synthesis that were found to be increased in lung cancer bearing animals.
Piperine could effectively inhibit B(a)P-induced lung carcinogenesis in albino mice by offering protection from protein damage and also by suppressing cell proliferation.
肺癌的统计数据促使人们迫切需要开发新的方法来控制这种最致命的癌症形式。化学预防就是这些新方法之一。香烟烟雾中的致癌物构成了尼古丁成瘾与肺癌之间的联系。与此同时，越来越明显的是，饮食和基因决定的因素在调节个体易感性方面发挥着重要作用，并且与化学预防方法相关。在本研究中，对胡椒碱预防小鼠肺癌发生的能力进行了表征，并确定了其对细胞增殖和蛋白质损伤生物标志物的影响。
将30只瑞士白化小鼠分成五组，每组6只动物。第一组动物口服玉米油作为对照。第二组动物每周两次给予50mg/kg体重的苯并(a)芘（B(a)P），连续4周，以便在第16周结束时诱发肺癌。第三组在给予第一剂致癌物后立即每隔一天给予50mg/kg体重的胡椒碱，持续16周。第四组也如第三组一样给予胡椒碱，但从B(a)P诱导的第6周开始直至实验结束。第五组动物作为药物对照，仅接受胡椒碱。
给予胡椒碱可显著降低在患肺癌动物中发现升高的脂质过氧化、蛋白质羰基、核酸含量和多胺合成水平。
胡椒碱可通过防止蛋白质损伤以及抑制细胞增殖，有效抑制B(a)P诱导的白化小鼠肺癌发生。
