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Grape seed proanthocyanidin inhibits inflammatory responses in hepatic stellate cells by modulating the MAPK, Akt and NF-kappa B signaling pathways

Authors
Lee, Jin-WooKim, Young IlKim, YoungchulChoi, MinjiMin, SeoyeonJoo, Yong HoonYim, Sung-VinChung, Namhyun
Issue Date
7월-2017
Publisher
SPANDIDOS PUBL LTD
Keywords
cyclooxygenase-2; grape seed proanthocyanidin; hepatic stellate cells; inducible nitric oxide synthase; mitogen-activated protein kinase; Toll-like receptors
Citation
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.40, no.1, pp.226 - 234
Indexed
SCIE
SCOPUS
Journal Title
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
Volume
40
Number
1
Start Page
226
End Page
234
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/82934
DOI
10.3892/ijmm.2017.2997
ISSN
1107-3756
Abstract
In the present study, we aimed to investigate the molecular mechanisms and prophylactic effects of grape seed proanthocyanidin (GSP) on lipopolysaccharide (LPS)-stimulated human hepatic stellate cells (HSCs). Cell counting and MTT assays were used to assess cell viability in the absence or presence of GSP. Reverse transcription-quantitative PCR (RT-qPCR) was performed for several inflammation-related genes (NOD1, NOD2, TLR2, TLR4, IL-1 , IL-6, IL-8, iNOS and COX-2). The expression of anti-inflammatory cell signaling molecules, including c-Jun N-terminal kinase (JNK), p38, extracellular signal regulated kinase (ERK), Akt, nuclear factor-B (NF-B), inhibitory-B (IB), iNOS and COX-2, was evaluated by western blot analysis. Finally, IL-8 levels in the culture supernatant of HSCs were measured by ELISA. Pretreatment with GSP before LPS treatment significantly suppressed the mRNA expression of pro-inflammatory cytokines such as IL-1, IL-6 and IL-8. GSP inhibited mRNA expression of LPS-induced TLR4, NOD2 and COX-2, in addition to inhibiting the expression of iNOS. GSP also inhibited LPS-induced NF-B activation and IB phosphorylation. Concomitantly, GSP dose-dependently suppressed the activation of MAP kinases (JNK, ERK and p38) and Akt in LPS-stimulated HSCs. These data suggest that GSP inhibits inflammatory responses in HSCs by inactivating the NF-B signaling pathway via MAP kinases. Thus, GSP may be considered as a novel drug for the treatment of hepatic inflammation, infectious diseases and fibrosis.
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