Rao Yerra Koteswara, Fang Shih-Hua, Tzeng Yew-Min
Institute of Biotechnology, Chaoyang University of Technology, Wufeng 413, Taiwan, ROC.
J Ethnopharmacol. 2007 Oct 8;114(1):78-85. doi: 10.1016/j.jep.2007.07.028. Epub 2007 Aug 2.
The extracts of chloroform (1) and methanol (2) from Antrodia camphorata (AC), and chloroform (3) and n-butanol (4) fractions of methanol extract from Cordyceps sinensis (CS), and hexane (5), ethyl acetate (6), and methanol (7) from Cinnamomum osmophloeum bark (CO) were evaluated for their anti-inflammatory as well as tumor-cell growth inhibitory activities in vitro. All the tested extracts dose dependently inhibited the enhanced production of inflammatory mediators such as nitric oxide (NO) through reducing inducible NO synthase expression, and cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-12 in LPS/IFN-gamma activated murine peritoneal macrophages. In addition, extracts 1 from AC, and 5 and 6 from CO significantly arrest the mitogen-stimulated spleen cells in G0/G1 stage. On the other hand, all these extracts were also evaluated for their tumor-cell proliferation activities in different type of cancer cell lines such as Jurkat, HepG2, PC 3, Colon 205, and MCF 7 as well as normal PBMCs. Compared to untreated controls, the extracts 1, 2, and 4-7 were most active and inhibited Jurkat cells with IC50 value of 22, 40, 18, 4, 5, and 45 microg/ml, respectively. In addition, the extracts 5, 6, and 7 from CO showed potent growth inhibition of HepG2 and PC 3 with IC50 values of 35, 80, 55 microg/ml; and 42, 125, and 50 microg/ml, respectively. Similarly, the extracts 1 and 5 inhibited the growth of Colon 205 and MCF 7 cells with IC50 values of 65, 33; and 95 and 30 microg/ml, respectively. Interestingly, none of the tested extract has shown cytotoxicity towards normal PBMCs up to the concentration range studies (0-150 microg/ml). Taken together, these data suggest that the anti-inflammatory and anti-cancer properties of AC, CS, and CO might result from the growth inhibition of NO, TNF-alpha and IL-12, and tumor cells proliferation, respectively.
对樟芝（AC）的氯仿提取物（1）和甲醇提取物（2）、冬虫夏草（CS）甲醇提取物的氯仿馏分（3）和正丁醇馏分（4）以及沉水樟树皮（CO）的己烷提取物（5）、乙酸乙酯提取物（6）和甲醇提取物（7）进行了体外抗炎和肿瘤细胞生长抑制活性评估。所有测试提取物均呈剂量依赖性地抑制炎症介质如一氧化氮（NO）的过量产生，其机制是通过降低诱导型NO合酶的表达来实现的，同时还能抑制脂多糖/γ干扰素激活的小鼠腹腔巨噬细胞中细胞因子（肿瘤坏死因子（TNF）-α和白细胞介素（IL）-12）的产生。此外，AC的提取物1以及CO的提取物5和6能显著使丝裂原刺激的脾细胞停滞于G0/G1期。另一方面，还对所有这些提取物在不同类型癌细胞系（如Jurkat、HepG2、PC 3、结肠205和MCF 7）以及正常外周血单个核细胞（PBMCs）中的肿瘤细胞增殖活性进行了评估。与未处理的对照相比，提取物1、2和4 - 7活性最强，对Jurkat细胞的IC50值分别为22、40、18、4、5和45微克/毫升。此外，CO的提取物5、6和7对HepG2和PC 3细胞显示出较强的生长抑制作用，IC50值分别为35、80、55微克/毫升；以及42、125和50微克/毫升。同样，提取物1和5对结肠205和MCF 7细胞的生长也有抑制作用，IC50值分别为65、33；以及95和30微克/毫升。有趣的是，在所研究的浓度范围内（0 - 150微克/毫升），没有一种测试提取物对正常PBMCs显示出细胞毒性。综上所述，这些数据表明，AC、CS和CO的抗炎和抗癌特性可能分别源于对NO、TNF - α和IL - 12的生长抑制以及肿瘤细胞增殖的抑制。
