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从台湾泡桐(Turpinia formosana Nakai)中分离得到细胞毒苯丙素类化合物和一种新的三萜酸,turformosinic 酸。

Cytotoxic phenylpropanoids and a new triterpene, turformosinic acid, from Turpinia formosana Nakai.

机构信息

School of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 404, Taiwan.

出版信息

Molecules. 2012 Feb 14;17(2):1837-51. doi: 10.3390/molecules17021837.

DOI:10.3390/molecules17021837
PMID:22334062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6268649/
Abstract

One new phenylpropanoid, turformosin A (1), and one new triterpene, turformosinic acid (2), together with 16 known compounds, were isolated from the stems of Turpinia formosana Nakai. All structures were elucidated on the basis of spectroscopic analysis, including 1D- and 2D-NMR techniques and MS analysis. Selected isolated compounds were evaluated for in vitro cytotoxicity against four human cancer cell lines and antioxidant scavenging effects on DPPH. (-)-(7'S,8'S)-threo-carolignan X (3) exhibited cytotoxicity against Hep2, WiDr, Daoy, and MCF-7 cell lines with ED(50) values of 3.60, 4.45, 6.07, and 13.7 μg/mL, respectively. Turformosin A (1), (-)-(7'S,8'S)- threo-carolignan X (3), methoxyhydroquinone-4-β-D-glucopyranoside (5), and methoxy-hydroquinone-1-β-D-glucopyranoside (6), exhibited similar anti-oxidative activity. Hep2 cells treated with 10 μg/mL of 3 showed elevation of sub-G1 population (from 20% at 8 h to 60% at 48 h), and activation of caspase-9/caspase-3/PARP cascade. Compound 3 induced intrinsic apoptotic pathway in Hep2 cells with dose and time dependence (10 μg/mL for 8 h).

摘要

从台湾泡桐(Turpinia formosana Nakai)的茎中分离得到了一个新的苯丙素类化合物 turformosin A(1)和一个新的三萜酸化合物 turformosinic acid(2),以及 16 个已知化合物。所有结构均基于光谱分析,包括 1D 和 2D-NMR 技术和 MS 分析进行阐明。选择分离得到的化合物对 4 个人类癌细胞系进行体外细胞毒性评估,并对 DPPH 进行抗氧化清除作用。(-)-(7'S,8'S)-threo-卡罗林烷 X(3)对 Hep2、WiDr、Daoy 和 MCF-7 细胞系表现出细胞毒性,ED(50)值分别为 3.60、4.45、6.07 和 13.7 μg/mL。Turformosin A(1)、(-)-(7'S,8'S)-threo-卡罗林烷 X(3)、甲氧基对苯二酚-4-β-D-吡喃葡萄糖苷(5)和甲氧基对苯二酚-1-β-D-吡喃葡萄糖苷(6)表现出相似的抗氧化活性。用 10 μg/mL 的 3 处理 Hep2 细胞,导致 sub-G1 群体(从 8 小时的 20%增加到 48 小时的 60%)增加,并且激活了 caspase-9/caspase-3/PARP 级联。化合物 3 以剂量和时间依赖性方式诱导 Hep2 细胞发生内在凋亡途径(10 μg/mL 作用 8 小时)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/6280d152fcea/molecules-17-01837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/1194a5b792e9/molecules-17-01837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/564a6df22c5e/molecules-17-01837-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/1c84cd70d16d/molecules-17-01837-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/6280d152fcea/molecules-17-01837-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/1194a5b792e9/molecules-17-01837-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/564a6df22c5e/molecules-17-01837-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/1c84cd70d16d/molecules-17-01837-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797f/6268649/6280d152fcea/molecules-17-01837-g004.jpg

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