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  4. Litchi (Litchi chinensis Sonn.) flower proanthocyanidin fraction exhibited protective efficacy to suppress nickel-induced expression for vascular endothelial growth factor in HepG2 cells
 
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Litchi (Litchi chinensis Sonn.) flower proanthocyanidin fraction exhibited protective efficacy to suppress nickel-induced expression for vascular endothelial growth factor in HepG2 cells

Journal
Journal of Food Biochemistry
Journal Volume
43
Journal Issue
7
Date Issued
2019-07-01
Author(s)
Lin, Jau Tien
Chang, Yuan Yen
YI-CHEN CHEN  
Liao, Po Lin
Yang, Deng Jye
DOI
10.1111/jfbc.12882
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85065241511&doi=10.1111%2fjfbc.12882&partnerID=40&md5=0b10e44aaf927d94af32ba7f4952c3c1
https://scholars.lib.ntu.edu.tw/handle/123456789/630243
URL
https://api.elsevier.com/content/abstract/scopus_id/85065241511
Abstract
The protective efficacy of litchi (Litchi chinensis Sonn.) flower proanthocyanidin fraction (LFPF) composed of (-)-epicatechin and proanthocyanidin A2 against vascular endothelial growth factor (VEGF) generation induced by nickel (Ni) in hepatocellular carcinoma (Hep G2) cells was studied. VEGF is an angiogenic inducer, which promotes tumor angiogenesis, leading to rapid tumor growth and metastasis. VEGF could be substantially induced in the Ni-mediated Hep G2 cells. Through LFPF treatment, the Ni-induced VEGF generation could be suppressed significantly. The inhibition of HIF-1α expression by blocking phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathways, and the suppression of Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT 3), and Raf-1 proto-oncogene, serine/threonine kinase (RAF1)/mitogen-activated protein kinase (MEK1/2)/extracellular-signal-regulated kinase (ERK1/2) pathways are important molecular mechanisms for the LFPF action. LFPF should probably reduce the risk of liver cancer in Ni-contaminated environments by inhibiting VEGF expression. Practical applications: LFPF mainly contained (-)-epicatechin and proanthocyanidin A2. Our results demonstrated that LFPF considerably suppressed the Ni-induced VEGF expression through inhibition of JAK2/STAT 3 and RAF1/MEK1/2/ERK1/2 pathways and prohibited HIF-1α expression through blocking PI3K/AKT/mTOR pathway. Litchi flowers might have the potential to diminish the liver cancer risk in a Ni-contaminated environment through suitable treatment.
Subjects
HepG2 cell; hypoxia inducible factor (HIF)-1α; litchi flower; mechanism; nickel (Ni); proanthocyanidin; vascular endothelial growth factor (VEGF)
Publisher
WILEY
Type
journal article

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