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Molecules 2014, 19(12), 19892-19906; doi:10.3390/molecules191219892

Maslinic Acid Induces Mitochondrial Apoptosis and Suppresses HIF-1α Expression in A549 Lung Cancer Cells under Normoxic and Hypoxic Conditions

1
Department of Respiratory Therapy, China Medical University, Taichung 40402, Taiwan
2
Department of Internal Medicine, China Medical University Hospital, Taichung 40402, Taiwan
3
Department of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan
4
Institute of Medicinal Chemistry and Department of Chemistry, East China Normal University, Shanghai 200241, China
5
Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China
6
Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan
7
Department of Nutrition, China Medical University, Taichung 40402, Taiwan
*
Author to whom correspondence should be addressed.
Received: 19 October 2014 / Revised: 20 November 2014 / Accepted: 21 November 2014 / Published: 28 November 2014
(This article belongs to the Section Medicinal Chemistry)
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Abstract

The apoptotic effects of maslinic acid (MA) at 4, 8, 16, 32 and 64 μmol/L on human lung cancer A549 cells under normoxic and hypoxic conditions were examined. MA at 4–64 and 16–64 μmol/L lowered Bcl-2 expression under normoxic and hypoxic conditions, respectively (p < 0.05). This agent at 4–64 μmol/L decreased Na+-K+-ATPase activity and increased caspase-3 expression under normoxic conditions, but at 8–64 μmol/L it caused these changes under hypoxic conditions (p < 0.05). MA up-regulated caspase-8, cytochrome c and apoptosis-inducing factor expression under normoxic and hypoxic conditions at 8–64 μmol/L and 32–64 μmol/L, respectively (p < 0.05). MA down-regulated hypoxia-inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), survivin and inducible nitric oxide synthase (iNOS) expression under normoxic and hypoxic conditions at 8–64 and 16–64 μmol/L, respectively (p < 0.05). After cells were pre-treated with YC-1, an inhibitor of HIF-1α, MA failed to affect the protein expression of HIF-1α, VEGF, survivin and iNOS (p > 0.05). MA at 8-64 and 32-64 μmol/L reduced reactive oxygen species and nitric oxide levels under both conditions (p < 0.05). These findings suggest that maslinic acid, a pentacyclic triterpenic acid, exerted its cytotoxic activities toward A549 cells by mediating mitochondrial apoptosis and the HIF-1α pathway. View Full-Text
Keywords: maslinic acid; lung cancer; HIF-1α; mitochondrial apoptosis maslinic acid; lung cancer; HIF-1α; mitochondrial apoptosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Hsia, T.-C.; Liu, W.-H.; Qiu, W.-W.; Luo, J.; Yin, M.-C. Maslinic Acid Induces Mitochondrial Apoptosis and Suppresses HIF-1α Expression in A549 Lung Cancer Cells under Normoxic and Hypoxic Conditions. Molecules 2014, 19, 19892-19906.

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