劉博仁醫師．營養功能醫學部落格

劉博仁醫師

台北菁英診所功能醫學抗老中心

台中市澄清醫院中港院區營養醫學門診主任

科瑩健康事業顧問醫師

    相當多乳癌患者前來我營養醫學門診諮詢抗癌營養療法。其中乳癌病理報告是ER陽性的戰友，醫師都會建議服用泰莫西芬 (tamoxifen)這種抗雌激素受體藥物，我也經常建議癌友攝取十字花科吲哚萃取物I3C，以幫助抗癌，I3C可以促進雌激素代謝物由壞的4羥以及16羥轉往好的2羥代謝物，幫助排毒以及代謝塑化劑，好處很多。

    問題是許多癌友問我：『乳癌患者服用抗賀爾蒙藥物泰莫西芬，會不會與吲哚萃取物I3C互相干擾？』

問得好，以下這篇2007年的研究發現，I3C本身不但有抗癌效果，還會加強泰莫西芬的抗癌效應。

    所以簡單說，目前證據是I3C不會干擾泰莫西芬抗癌效應，甚至還有加強其抗癌效果的效果。

Eur J Cancer Prev. 2007 Apr;16(2):130-41.

Suppression of mammary gland carcinogenesis by post-initiation treatment of rats with tamoxifen or indole-3-carbinol or their combination.

Malejka-Giganti D1, Parkin DR, Bennett KK, Lu Y, Decker RW, Niehans GA, Bliss RL.

Abstract

This study examined whether suppression of mammary gland carcinogenesis elicited by low doses of tamoxifen (TAM) can be enhanced by concomitant treatment of rats with indole-3-carbinol (I3C), a component of cruciferous vegetables and a dietary supplement used for its putative antiestrogenicity. Two weeks after one oral dose of 7,12-dimethylbenz[a]anthracene (DMBA) at 65 mg/kg body weight, female Sprague-Dawley rats started treatment with TAM (10 microg/rat) by subcutaneous injection, I3C (250 mg/kg body weight) by oral gavage, TAM+I3C or their respective vehicles three times per week, for up to 20 weeks. Significant increases in the median latency of malignant mammary tumors and decreases in the mean tumor mass per rat were due to TAM. Significant decreases in the mean tumor number per rat in TAM, I3C and TAM+I3C-treated rats indicated a cooperative effect of the two compounds. In both DMBA-initiated and uninitiated rats, significant increases in the ratios of liver to body weight in I3C and TAM+I3C-treated groups coincided with I3C-dependent increases of hepatic cytochrome P450 levels and activities (1A1, 1A2 and 2B1/2). The ratios of uterus to body weight decreased with the number of treatments and the decreases effected by TAM were greater than those by I3C. The levels of circulating estrone were increased in response to I3C treatment and were greater in DMBA-initiated rats than in uninitiated rats, which may contribute to the preventive effect of I3C. Chemoprevention may be accomplished through up-regulation of apoptotic enzyme (caspase) activities in the mammary gland or mammary tumors. Treatment with TAM, I3C or TAM+I3C had no effect on caspase-3&7, caspase-6, caspase-8 and caspase-9 activities in the mammary tumors or mammary gland of tumor-bearing rats or that of uninitiated rats. In the mammary gland of DMBA-initiated tumor-free rats, however, I3C treatment increased the levels of caspase-3&7 and caspase-9 activities, suggesting an I3C-mediated protective effect. Even though I3C alone is a much less effective suppressing agent of mammary carcinogenesis than TAM, I3C in combination with TAM does not weaken but may foster the benefits of chemoprevention with TAM.