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2
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Chin J Cancer Res. 2012 Jun;24(2):109-15. doi: 10.1007/s11670-012-0109-8.
2
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Curr Drug Targets. 2012 Dec;13(14):1730-7. doi: 10.2174/138945012804545623.
3
Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid inhibits hepatocellular carcinoma in vitro and in vivo via stabilizing IkBα.表松脂烷-11α-羟基-15-氧代-贝壳杉-16-烯-19-酸通过稳定 IkBα 抑制肝癌的体内外活性。
Invest New Drugs. 2012 Dec;30(6):2210-8. doi: 10.1007/s10637-011-9791-5. Epub 2012 Jan 7.
4
[Effect of Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid on human gastric cancer cells and its mechanism].内-11α-羟基-15-氧代-贝壳杉-16-烯-19-酸对人胃癌细胞的作用及其机制
Nan Fang Yi Ke Da Xue Xue Bao. 2011 Aug;31(8):1345-8.
5
Anticancer efficacy of 5F in NNK-induced lung cancer development of A/J mice and human lung cancer cells.5F 在 NNK 诱导的 A/J 小鼠肺癌发生和人肺癌细胞中的抗癌功效。
J Mol Med (Berl). 2010 Dec;88(12):1265-76. doi: 10.1007/s00109-010-0676-4. Epub 2010 Sep 10.
6
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The role of Ca2+ on the DADS-induced apoptosis in mouse-rat hybrid retina ganglion cells (N18).钙离子对二烯丙基二硫化物（DADS）诱导的小鼠-大鼠杂交视网膜神经节细胞（N18）凋亡的作用。
Neurochem Res. 2006 Mar;31(3):383-93. doi: 10.1007/s11064-005-9035-1. Epub 2006 May 3.
8
Phenethyl isothiocyanate and sulforaphane and their N-acetylcysteine conjugates inhibit malignant progression of lung adenomas induced by tobacco carcinogens in A/J mice.苯乙基异硫氰酸酯和萝卜硫素及其N-乙酰半胱氨酸共轭物可抑制A/J小鼠中由烟草致癌物诱导的肺腺瘤的恶性进展。
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Over-expression of Bcl-2 against Pteris semipinnata L-induced apoptosis of human colon cancer cells via a NF-kappa B-related pathway.Bcl-2过表达通过NF-κB相关途径抑制半边旗诱导的人结肠癌细胞凋亡。
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Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer.卵巢癌中通过降低半胱天冬酶-3活性和抗凋亡蛋白过表达来抵抗化疗诱导的细胞凋亡。
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5F对A/J小鼠肺癌发生的抑制作用。

Inhibitory effect of 5F on development of lung cancer in A/J mice.

作者信息

Ye Hua, Yang Xiaoqing, Wu Kefeng, Li Li, Lv Yingnian, Liu Yi, Zheng Xuebao

机构信息

Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College Zhanjiang 524023, Guangdong Province, China.

出版信息

Int J Clin Exp Pathol. 2015 Apr 1;8(4):4138-42. eCollection 2015.

PMID:26097604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4466991/
Abstract

The purpose of the study is to investigate the effect of ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) on the model of induced A/J mice lung cancer in A/J mice. The expressions of tumor-related molecules including P65 and Bcl-2 at protein level were examined using the immunohistochemical method (IHC). Side effects of 5F were also monitored. The results indicated that 5F significantly suppressed the development of B[a]P and NNK-induced lung cancer in vivo by facilitating cell apoptosis with minimal side effects. Compared to the expressions of P65 and Bcl-2 in model group, the levels were strongly attenuated both in blank and 5F injection groups. Moreover, P65 and Bcl-2 levels varied among different groups receiving 5F treatment. The expressions of P65 and Bcl-2 were much lower in groups receiving high-concentration 5F treatment than those with low-concentration 5F injection. Findings revealed that 5F inhibited the pathogenesis of lung cancer through accelerating apoptosis in a dose-dependent manner.

摘要

本研究旨在探讨ent-11α-羟基-15-氧代-贝壳杉-16-烯-19-酸（5F）对A/J小鼠诱发性肺癌模型的影响。采用免疫组织化学方法（IHC）检测包括P65和Bcl-2在内的肿瘤相关分子在蛋白水平的表达。同时监测5F的副作用。结果表明，5F通过促进细胞凋亡在体内显著抑制苯并[a]芘和NNK诱导的肺癌发展，且副作用最小。与模型组相比，空白组和5F注射组中P65和Bcl-2的表达水平均显著降低。此外，接受5F治疗的不同组中P65和Bcl-2水平有所不同。接受高浓度5F治疗组的P65和Bcl-2表达远低于低浓度5F注射组。研究结果表明，5F通过以剂量依赖方式加速细胞凋亡来抑制肺癌的发病机制。