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奥克美辛甘水提取物诱导肺腺癌细胞 A549 发生凋亡信号转导。

Ocimum gratissimum Aqueous Extract Induces Apoptotic Signalling in Lung Adenocarcinoma Cell A549.

机构信息

Department of Life Science, Fu-Jen Catholic University, Taipei 24205, Taiwan.

出版信息

Evid Based Complement Alternat Med. 2011;2011. doi: 10.1155/2011/739093. Epub 2010 Sep 26.

DOI:10.1155/2011/739093
PMID:20953389
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2952322/
Abstract

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.

摘要

奥克西姆 gratissimum(OG)广泛用作一种传统草药,具有抗菌活性在台湾。最近,OG 的抗肿瘤作用也有报道乳腺癌细胞;然而,OG 对人肺腺癌细胞 A549 的影响尚不清楚。因此,我们旨在探讨奥格是否水溶液提取物(OGE)影响 A549 细胞活力和 OGE 在 A549 细胞中诱导的信号。细胞活力测定表明,OGE 显著且剂量依赖性地降低了 A549 细胞的活力,但对 BEAS-2B 细胞没有影响。形态学检查和 DAPI 染色表明,OGE 诱导 A549 细胞细胞收缩和 DNA 凝聚。进一步的研究表明,OGE 增强了 caspase-3、caspase-9 和 caspase-8 的激活,并增加了 Apaf-1 和 Bak 的蛋白水平,但降低了 Bcl-2 的水平。此外,OGE 抑制了细胞外信号调节激酶(ERK)的磷酸化,而增强了 c-Jun N-末端激酶(JNK)和 p38 丝裂原活化蛋白激酶(p38)的磷酸化。总之,我们的研究结果表明,OGE 抑制了 A549 细胞的活力,这可能是由于凋亡信号的激活和抗凋亡信号的抑制所致,提示 OGE 可能有益于肺癌的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6601/2952322/97e7ed28ac6f/ECAM2011-739093.007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6601/2952322/6fa4f6a71a2e/ECAM2011-739093.002.jpg
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