Inhibitory effects of black tea, green tea, decaffeinated black tea, and decaffeinated green tea on ultraviolet B light-induced skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated SKH-1 mice.
Inhibitory effects of black tea, green tea, decaffeinated black tea, and decaffeinated green tea on ultraviolet B light-induced skin carcinogenesis in 7,12-dimethylbenz[a]anthracene-initiated SKH-1 mice.
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发表时间：
1994-07
期刊：
影响因子：
11.2
通讯作者：
Z. Y. Wang;Mou-tuan Huang;Y. Lou;Jian-Guo Xie;K. Reuhl;H. Newmark;Chi-Tang Ho;Chung S. Yang;A. Conney
中科院分区：
文献类型：
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作者：
Z. Y. Wang;Mou-tuan Huang;Y. Lou;Jian-Guo Xie;K. Reuhl;H. Newmark;Chi-Tang Ho;Chung S. Yang;A. Conney
在以前的研究中（Z。Y. Wang等人，癌症研究所，五十二：1162-1170，1992），我们发现给予绿色茶叶的水提取物作为饮用流体的唯一来源抑制了先前用7，12-二甲基苯并[a]蒽（DMBA）引发的SKH-1小鼠中紫外线B光（UVB）诱导的致癌作用。在本研究中，我们比较了红茶，绿色茶，脱咖啡因红茶，脱咖啡因绿色茶对UVB诱导的皮肤癌发生在DMBA启动的SKH-1小鼠。通过在邦恩茶冲泡机中使4升热水通过50 g茶叶来制备每种茶叶的1.25%水提取物（1.25 g茶叶/100 ml水）。在本研究过程中分析的1.25%红茶、绿色茶、脱咖啡因红茶和脱咖啡因绿色茶的多个样品中固体的平均浓度分别为4.23、3.94、3.66和3.53 mg/ml。这些茶固体的浓度与人类摄入的茶冲泡物中存在的浓度相似。用200 nmol DMBA局部处理雌性SKH-1小鼠，3周后用30 mJ/cm 2 UVB每周照射两次，持续31周。UVB诱导的皮肤肿瘤的形成被显着抑制口服给药的0.63或1.25%的红茶，绿色茶，脱咖啡因红茶，或脱咖啡因绿色茶作为唯一的饮用液体来源2周前和31周的UVB治疗。八种茶制剂中的每一种的施用不仅抑制了肿瘤的数量，而且肿瘤的大小也显著减小。每个肿瘤的组织学检查表明，口服八种茶制剂对UVB诱导的角化棘皮瘤和癌的形成具有显着的抑制作用。给予1.25%红茶、绿色茶、脱咖啡因红茶或脱咖啡因绿色茶，每只小鼠的角化棘皮瘤数量分别抑制79、78、73或70%，每只小鼠的癌数量分别抑制93、88、77或72%。总之，红茶的管理是可比的绿色茶作为UVB诱导的皮肤癌的抑制剂在DMBA启动的SKH-1小鼠。口服脱咖啡因的红茶或脱咖啡因的绿色茶也有显着的抑制作用，UVB诱导的皮肤癌发生在DMBA启动的SKH-1小鼠，但这些茶制剂在高剂量水平的效果略低于常规茶。
In a previous study (Z. Y. Wang et al., Cancer Res., 52: 1162-1170, 1992), we found that administration of a water extract of green tea leaves as the sole source of drinking fluid inhibited ultraviolet B light (UVB)-induced carcinogenesis in SKH-1 mice previously initiated with 7,12-dimethylbenz[a]anthracene (DMBA). In the present study, we compared the effects of black tea, green tea, decaffeinated black tea, and decaffeinated green tea on UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice. A 1.25% water extract of each kind of tea leaf (1.25 g tea leaf/100 ml water) was prepared by passing 4 liters of hot water through 50 g of tea leaves in a Bunn tea brewing machine. The mean concentrations of solids in multiple samples of 1.25% black tea, green tea, decaffeinated black tea, and decaffeinated green tea analyzed during the course of this study were 4.23, 3.94, 3.66, and 3.53 mg/ml, respectively. These concentrations of tea solids are similar to those present in tea brews ingested by humans. Female SKH-1 mice were treated topically with 200 nmol of DMBA, followed 3 weeks later by irradiation with 30 mJ/cm2 of UVB twice weekly for 31 weeks. UVB-induced formation of skin tumors was markedly inhibited by oral administration of 0.63 or 1.25% black tea, green tea, decaffeinated black tea, or decaffeinated green tea as the sole source of drinking fluid 2 weeks prior to and during 31 weeks of UVB treatment. Administration of each of the eight tea preparations not only inhibited the number of tumors, but tumor size was also markedly decreased. Histopathological examination of each tumor showed that oral administration of the eight tea preparations had a marked inhibitory effect on the formation of UVB-induced keratoacanthomas and carcinomas. Administration of 1.25% black tea, green tea, decaffeinated black tea, or decaffeinated green tea inhibited the number of keratoacanthomas per mouse by 79, 78, 73, or 70%, respectively, and the number of carcinomas per mouse was inhibited by 93, 88, 77, or 72%, respectively. In summary, administration of black tea was comparable to green tea as an inhibitor of UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice. Oral administration of decaffeinated black tea or decaffeinated green tea also had a marked inhibitory effect on UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice, but these tea preparations were slightly less effective than the regular teas at the high dose level.