title: A new function of green tea: prevention of lifestyle-related diseases.
abstract: In the normal human life span, there occur lifestyle-related diseases that may be preventable with nontoxic agents. This paper deals with the preventive activity of green tea in some lifestyle-related diseases. Green tea is one of the most practical cancer preventives, as we have shown in various in vitro and in vivo experiments, along with epidemiological studies. Among various biological effects of green tea, we have focused on its inhibitory effect on TNF-alpha gene expression mediated through inhibition of NF-kappaB and AP-1 activation. Based on our recent results with TNF-alpha-deficient mice, TNF-alpha is an endogenous tumor promoter. TNF-alpha is also known to be a central mediator in chronic inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. We therefore hypothesized that green tea might be a preventive agent for chronic inflammatory diseases. To test this hypothesis, TNF-alpha transgenic mice, which overexpress TNF-alpha only in the lungs, were examined. The TNF-alpha transgenic mouse is an animal model of human idiopathic pulmonary fibrosis which also frequently develops lung cancer. Expressions of TNF-alpha and IL-6 were inhibited in the lungs of these mice after treatment with green tea in drinking water for 4 months. In addition, judging from the results of a prospective cohort study in Saitama Prefecture, Japan, green tea helps to prevent cardiovascular disease. In this study, a decreased relative risk of death from cardiovascular disease was found for people consuming over 10 cups of green tea a day, and green tea also had life-prolonging effects on cumulative survival. These data suggest that green tea has preventive effects on both chronic inflammatory diseases and lifestyle-related diseases (including cardiovascular disease and cancer), resulting in prolongation of life span.
authors.affiliation: Saitama Cancer Center Research Institute, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Sueoka
authors.forename: M
authors.initials: M
authors.lastname: Suganuma
authors.forename: E
authors.initials: E
authors.lastname: Sueoka
authors.forename: S
authors.initials: S
authors.lastname: Okabe
authors.forename: S
authors.initials: S
authors.lastname: Matsuyama
authors.forename: K
authors.initials: K
authors.lastname: Imai
authors.forename: K
authors.initials: K
authors.lastname: Nakachi
authors.forename: H
authors.initials: H
authors.lastname: Fujiki
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology / Q000627:therapeutic use; D002273:Carcinogens / Q000633:toxicity; D002318:Cardiovascular Diseases / Q000401:mortality / Q000517:prevention & control; D002392:Catechin / Q000031:analogs & derivatives / Q000302:isolation & purification / Q000627:therapeutic use; D015331:Cohort Studies; D006224:Cricetinae; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D007564:Japan / Q000453:epidemiology; D008019:Life Style; D008168:Lung / Q000378:metabolism; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D016328:NF-kappa B / Q000378:metabolism; D009374:Neoplasms, Experimental / Q000517:prevention & control; D019319:Okadaic Acid / Q000633:toxicity; D008517:Phytotherapy; D011322:Primary Prevention; D011446:Prospective Studies; D011658:Pulmonary Fibrosis / Q000188:drug therapy / Q000378:metabolism; D051381:Rats; D012306:Risk; D013662:Tea / Q000737:chemistry; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics
chemical_list: D016588:Anticarcinogenic Agents; D002273:Carcinogens; D015850:Interleukin-6; D016328:NF-kappa B; D013662:Tea; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D019319:Okadaic Acid; D002392:Catechin; C045651:epigallocatechin gallate