Ye Hua, Yang Xiaoqing, Wu Kefeng, Li Li, Lv Yingnian, Liu Yi, Zheng Xuebao
Guangdong Key Laboratory for Research and Development of Natural Drugs, Guangdong Medical College Zhanjiang 524023, Guangdong Province, China.
Int J Clin Exp Pathol. 2015 Apr 1;8(4):4138-42. eCollection 2015.
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.
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。