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2017 ; 9
(4
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Suppression of Hepatic Epithelial-to-Mesenchymal Transition by Melittin via
Blocking of TGF?/Smad and MAPK-JNK Signaling Pathways
#MMPMID28406452
Park JH
; Park B
; Park KK
Toxins (Basel)
2017[Apr]; 9
(4
): ä PMID28406452
show ga
Transforming growth factor (TGF)-?1 plays a crucial role in the
epithelial-to-mesenchymal transition (EMT) in hepatocytes and hepatic stellate
cells (HSC), which contributes to the pathogenesis of liver fibrosis. Melittin
(MEL) is a major component of bee venom and is effective in rheumatoid arthritis,
pain relief, cancer cell proliferation, fibrosis and immune modulating activity.
In this study, we found that MEL inhibits hepatic EMT in vitro and in vivo,
regulating the TGF?/Smad and TGF?/nonSmad signaling pathways. MEL significantly
inhibited TGF-?1-induced expression of EMT markers (E-cadherin reduction and
vimentin induction) in vitro. These results were confirmed in CCl?-induced liver
in vivo. Treatment with MEL almost completely blocked the phosphorylation of
Smad2/3, translocation of Smad4 and phosphorylation of JNK in vitro and in vivo.
Taken together, these results suggest that MEL suppresses EMT by inhibiting the
TGF?/Smad and TGF?/nonSmad-c-Jun N-terminal kinase (JNK)/Mitogen-activated
protein kinase (MAPK) signaling pathways. These results indicated that MEL
possesses potent anti-fibrotic and anti-EMT properties, which may be responsible
for its effects on liver diseases.
|Animals
[MESH]
|Carbon Tetrachloride
[MESH]
|Cell Line
[MESH]
|Chemical and Drug Induced Liver Injury/drug therapy/metabolism
[MESH]