Ocimum gratissimum Aqueous Extract Induces Apoptotic Signalling in Lung Adenocarcinoma Cell A549
Han-Min Chen,1 Mu-Jang Lee,2 Cheng-Yi Kuo,3 Pei-Lin Tsai,4 Jer-Yuh Liu,5 and Shao-Hsuan Kao4,6,7
1Department of Life Science, Fu-Jen Catholic University, Taipei 24205, Taiwan
2Department of Internal Medicine, Division of Cardiology, Tian-Sheng Memorial Hospital, Pingtung 92843, Taiwan
3Multi Chemical Laboratory, SGS Taiwan Ltd., Taipei 24803, Taiwan
4Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung City 40201, Taiwan
5Graduate Institute of Cancer Biology, China Medical University and Hospital, Taichung City 40402, Taiwan
6Clinical Laboratory, Chung Shan Medical University Hospital, Taichung City 40201, Taiwan
7Institutes of Biochemistry and Biotechnology, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Road, Taichung 40201, Taiwan
Ocimum gratissimum (OG) is widely used as a traditional herb for its antibacterial activity in Taiwan. Recently, antitumor effect of OG on breast cancer cell is also reported; however, the effects of OG on human pulmonary adenocarcinoma cell A549 remain unclear. Therefore, we aimed to investigate whether aqueous OG extract (OGE) affects viability of A549 cells and the signals induced by OGE in A549 cells. Cell viability assays revealed that OGE significantly and dose-dependently decreased the viability of A549 cell but not that of BEAS-2B cell. Morphological examination and DAPI staining indicated that OGE induced cell shrinkage and DNA condensation for A549 cells. Further investigation showed that OGE enhanced activation of caspase-3, caspase-9 and caspase-8 and increased protein level of Apaf-1 and Bak, but diminished the level of Bcl-2. Additionally, OGE inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) yet enhanced the phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAP kinase (p38). In conclusion, our findings indicate that OGE suppressed the cell viability of A549 cells, which may result from the activation of apoptotic signaling and the inhibition of anti-apoptotic signaling, suggesting that OGE might be beneficial to lung carcinoma treatment.
....In conclusion, the present study provides evidences that OGE treatments significantly alter viability of lung adenocarcinoma A549 cells through a synergy of induction of apoptotic signaling and suppression of antiapoptotic signaling, as shown in Figure 7. Moreover, OGE treatment simultaneously inhibits the activation of ERK and enhances the activation of JNK and p38, which is consistent with the enhanced apoptotic signaling and reduced antiapoptotic signaling based on their well-known effects on these signal cascades (Figure 7). By manipulating both arms of apoptotic and antiapoptotic pathway, OGE represents a promisingly effective chemopreventive agent against lung adenocarcinoma.
Source :Evidence-Based Complementary and Alternative Medicine Volume 2011 (2011), Article ID 739093, 7 pages
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