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

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Department of Respiratory Therapy, China Medical University, Taichung 40402, Taiwan
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Department of Internal Medicine, China Medical University Hospital, Taichung 40402, Taiwan
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Department of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan
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Institute of Medicinal Chemistry and Department of Chemistry, East China Normal University, Shanghai 200241, China
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Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China
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Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan
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Department of Nutrition, China Medical University, Taichung 40402, Taiwan
*
Author to whom correspondence should be addressed.
Molecules 2014, 19(12), 19892-19906; https://doi.org/10.3390/molecules191219892
Received: 19 October 2014 / Revised: 20 November 2014 / Accepted: 21 November 2014 / Published: 28 November 2014
(This article belongs to the Section Medicinal Chemistry)
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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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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