Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27330276
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Anti-inflammatory effects of guggulsterone on murine macrophage by inhibiting
LPS-induced inflammatory cytokines in NF-?B signaling pathway
#MMPMID27330276
Zhang JH
; Shangguan ZS
; Chen C
; Zhang HJ
; Lin Y
Drug Des Devel Ther
2016[]; 10
(?): 1829-35
PMID27330276
show ga
The present study was aimed to investigate the effects of guggulsterone (GS) on
proinflammatory responses as well as the underlying molecular mechanisms in
macrophage upon lipopolysaccharide (LPS) stimulation. Effects of GS on viability
of Raw264.7 cells were examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl
tetrazolium bromide (MTT) assay. Real-time polymerase chain reaction (PCR) was
employed to examine the mRNA expression of cytokines, including interleukin 1?
(IL-1?), tumor necrosis factor-alpha (TNF-?), and inducible nitric oxide synthase
(iNOS). Phosphorylations of extracellular signal-regulated kinase (ERK), c-Jun
N-terminal kinase (JNK), p38 mitogen-activated protein kinases (p38), and
inhibitor of nuclear factor kappaB (I?B) were determined using immunoblotting.
The results revealed that GS was not toxic to Raw264.7 cells at designated
concentrations. We demonstrated that GS significantly suppressed the elevated
mRNA expression of proinflammatory cytokines, including IL-1?, TNF-?, and iNOS in
a dose-dependent manner. GS treatment reduced the level of I?B phosphorylation in
LPS-stimulated macrophages in a dose-dependent manner. Use of BAY 11-7082, an
inhibitor of nuclear factor-kappaB (NF-?B), led to significantly suppressing
effects on IL-1? and TNF-? expression similar as that of GS-treated cells. Our
findings suggest that GS possesses anti-inflammatory activity, which may be
attributed to downregulation of iNOS and inhibition of NF-?B activity in
LPS-stimulated Raw264.7 cells.
free
free
free
