So-Cheong-Ryong-Tang induces apoptosis through activation of the intrinsic and extrinsic apoptosis pathways, and inhibition of the PI3K/Akt signaling pathway in non-small-cell lung cancer A549 cells

BMC Complementary and Alternative Medicine

Yung Hyun Choi¹  Gi-Young Kim²  Su Hyun Hong⁴  Cheol Park³ 

[1] Anti-Aging Research Center and Blue-Bio Industry RIC, Dongeui University, 176 Eomgwangno Busanjin-gu, Busan 614-714, Republic of Korea;Laboratory of Immunobiology, Department of Marine Life Sciences, Jeju National University, 102 Jejudaehak-ro, Jeju 690-756, Republic of Korea;Department of Molecular Biology, College of Natural Sciences, Dongeui University, 176 Eomgwangno Busanjin-gu, Busan 614-714, Republic of Korea;Department of Biochemistry, Dongeui University College of Korean Medicine, 52-57, Yangjeong-ro, Busanjin, Busan 614-052, Republic of Korea

关键词: PI3K/Akt;    Caspase;    Apoptosis;    A549 cells;    So-Cheong-Ryong-Tang;   

Others  :  1172050
DOI  :  10.1186/s12906-015-0639-y

 received in 2014-10-24, accepted in 2015-03-30,  发布年份 2015

【 摘 要 】

Background

So-Cheong-Ryong-Tang (SCRT), a traditional Korean medicine containing eight species of medicinal plant, has been used to treat patients with bronchial asthma and allergic rhinitis for hundreds of years; however, its anti-cancer potential is poorly understood. The present study was designed to evaluate the apoptotic effect of SCRT against human non-small-cell lung cancer (NSCLC) A549 cells.

Methods

The effects of SCRT on cell growth and viability were evaluated by trypan blue dye exclusion and 3-(4, 5-dimethyl-thiazol-2-yl)-2, 5-diphenyl tetrazoliumbromide (MTT) assays, respectively. Apoptosis was detected using 4,6-diamidino-2-phenyllindile (DAPI) staining, agarose gel electrophoresis and flow cytometry. The protein levels were determined by Western blot analysis. Caspase activity was measured using a colorimetric assay.

Results

SCRT treatment resulted in significantly decreased A549 cell growth and viability by induction of apoptosis. SCRT induced the translocation of pro-apoptotic Bax to the mitochondria, mitochondrial membrane permeabilization, cytochrome c release from mitochondria to cytosol, and activated caspase-9 and caspase-3. SCRT also increased death receptor-associated ligands and enhanced the activation of caspase-8 and cleavage of its substrate Bid. However, the pan-caspases inhibitor significantly blocked the SCRT-induced apoptosis, suggesting that it is a caspase-dependent pathway. In addition, SCRT suppressed the phosphorylation of phosphoinositide 3-kinase (PI3K) and Akt, and treatment with a potent inhibitor of PI3K further increased the apoptotic activity of SCRT.

Conclusions

These findings suggest that SCRT may play its anti-cancer actions partly through a suppression of the PI3K/Akt signal pathway in A549 cells, and further in vivo studies on the potential of SCRT for prevention and therapy of NSCLCs are warranted.

【 授权许可】

   
2015 Park et al.; licensee BioMed Central.

【 图 表 】

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