Anti-Tumor Effects of Atractylenolide I Isolated from Atractylodes macrocephala in Human Lung Carcinoma Cell Lines

被引:114
作者
Liu, Huanyi [1 ]
Zhu, Yajie [1 ]
Zhang, Tao [1 ]
Zhao, Zhenguo [1 ]
Zhao, Yu [1 ]
Cheng, Peng [1 ]
Li, Hua [1 ]
Gao, Hui [1 ]
Su, Xiaomei [1 ]
机构
[1] Chengdu Mil Gen Hosp, Dept Oncol, Chengdu 610083, Si Chuan Provin, Peoples R China
关键词
atractylenolide I; Atractylodes macrocephala; antitumor activity; apoptosis; lung cancer; HUMAN LEUKEMIA-CELLS; CYCLE ARREST; APOPTOSIS; SESQUITERPENOIDS; EMODIN; ADENOCARCINOMA; ACTIVATION; PATHWAY;
D O I
10.3390/molecules181113357
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Atractylenolide I (ATL-1) is the major sesquiterpenoid of Atractylodes macrocephala. This study was designed to investigate whether ATL-1 induced apoptosis in A549 and HCC827 cells in vitro and in vivo. In our results, ATL-1 significantly decreased the percentage of in vitro viability, in a dose-dependent manner. In addition, DAPI staining and flow cytometry tests demonstrated the induction of apoptosis by ATL-I. Western blot analysis indicated that the protein levels of caspase-3, caspase-9 and Bax were increased in A549 and HCC827 cells after ATL-I exposure; to the contrary, the expressions of Bcl-2, Bcl-XL were decreased after treatment with ATL-1. In the in vivo study, ATL-I effectively suppressed tumor growth (A549) in transplanted tumor nude mice with up-regulation of caspase-3, caspase-9, and Bax and down-regulation of Bcl-2 and Bcl-XL. In conclusion, our results demonstrated that ATL-I has significant antitumor activity in lung carcinoma cells, and the possible mechanism of action may be related to apoptosis induced by ATL-I via a mitochondria-mediated apoptosis pathway.
引用
收藏
页码:13357 / 13368
页数:12
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