Flufenamic acid promotes angiogenesis through AMPK activation

Ge,Ruiliang; Hu,Lei; Tai,Yilin; Xue,Feng; Yuan,Lei; Wei,Gongtian; Wang,Yi

doi:10.3892/ijo.2013.1891

Flufenamic acid promotes angiogenesis through AMPK activation

Authors:
- Ruiliang Ge
- Lei Hu
- Yilin Tai
- Feng Xue
- Lei Yuan
- Gongtian Wei
- Yi Wang
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Affiliations: Division of Hepatic Surgery Ⅱ, Eastern Hepatobiliary Hospital, Second Military Medical University, Shanghai 200438, P.R. China, Laboratory of Neural Signal Transduction, State Key Laboratory of Neuroscience, Institute of Neuroscience, Shanghai Institutes of Biological Sciences, Shanghai 200031, P.R. China
Published online on: April 10, 2013 https://doi.org/10.3892/ijo.2013.1891
Pages: 1945-1950

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Abstract

Angiogenesis plays critical roles in development, tumor growth and metastasis. Flufenamic acid (FFA) is an anti-inflammatory agent known to alter ion fluxes across the plasma membrane. Its role in angiogenesis has not been fully addressed to date. Here, we report that FFA treatment promotes angiogenesis both in vitro and in vivo. Applying FFA for 12 h promoted tube formation of human umbilical vein endothelial cells (HUVECs) without affecting cell proliferation. Three angiogenesis-related genes, VEGF, e-NOS and AAMP, were analyzed by RT-PCR. A significant difference was found between the FFA group and the control; the FFA group had significantly higher mRNA accumulation levels of all the three genes (p<0.05). Moreover, in the chick embryo chorioallantoic membrane (CAM) assay, FFA promoted the formation of macroscopic blood vessels. Finally, western blotting showed that the FFA-treated group had significantly higher phosphorylated AMPK levels, compared with the control (p<0.05). These results suggest that FFA promotes angiogenesis both in vitro and in vivo likely via promoting tube formation through AMPK activation.

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