In:
Experimental Biology and Medicine, SAGE Publications, Vol. 231, No. 4 ( 2006-04), p. 444-455
Kurzfassung:
The aim of this study is to elucidate the effects of Scutellaria baicalensis Georgi (SbG) extract and its constituents on macrophage-hepatocyte interaction in primary cultures. By using trans-well primary Kupffer cell culture or conditioned medium (CM) from murine macrophage RAW264.7 cell line (RAW cells), effects of SbG on hepatocyte growth were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide and trypan blue exclusion assay. Cytokine production, antibody-neutralization studies, and molecular mechanisms of transforming growth factor (TGF)-β1 gene expression were elucidated on SbG-treated RAW264.7 cells. In addition, recombinant human TGF-β1 (r-human TGF-β1) was added to elucidate the mechanisms of SbG effects on cultured hepatocytes. Immunohistochemistry using anti-NF-κB antibody was used to determine the possible signal transduction pathways in primary hepatocyte culture. The results showed that SbG stimulated the proliferation of cultured hepatocytes, possibly through NF-κB, but not of Toll-like receptor 4 activation; whereas SbG-RAW-CM and SbG in trans-well significantly suppressed the proliferation of hepatocytes. Antibody-neutralization studies revealed that TGF-β1 was the main antimitotic cytokine in SbG-treated RAW cells CM. The growth stimulation effect of SbG on cultured hepatocytes was inhibited by exogenous administration of r-human TGF-β1. Furthermore, SbG induced NF-κB translocation into the nuclei of cultured cells. In the RAW264.7 line, SbG and baicalin stimulated TGF-β1 gene expression via NF-κB and protein kinase C activation. We conclude that SbG stimulates hepatocyte growth via activation of the NF-κB pathway and induces TGF-β1 gene expression through the Kupffer cell–hepatocyte interaction, which subsequently results in the inhibition of SbG-stimulated hepatocyte growth.
Materialart:
Online-Ressource
ISSN:
1535-3702
,
1535-3699
DOI:
10.1177/153537020623100410
Sprache:
Englisch
Verlag:
SAGE Publications
Publikationsdatum:
2006
ZDB Id:
2020856-X
SSG:
12
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