[Show abstract][Hide abstract] ABSTRACT: Periodontitis, a chronic inflammatory periodontal disease that develops from gingivitis, is caused by periodontal pathogenic bacteria such as Porphyromonas gingivalis. Recent studies have focused on the antioxidant, anti-human immunodeficiency virus, anticarcinogenic, and anti-inflammatory properties of gomisins. However, the anti-inflammatory activities of gomisin plants through heme oxygenase-1 (HO-1) signals remain poorly defined. We found that gomisins' anti-inflammatory activity occurs via the induction of HO-1 expression. Gomisins G and J inhibit the production of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 and also block nuclear factor-κB activation in Raw264.7 cells stimulated with P. gingivalis lipopolysaccharide. Furthermore, pro-inflammatory cytokine production is inhibited through the induction of HO-1 expression. HO-1 expression is induced by all gomisins, but their anti-inflammatory activity via HO-1 signaling is observed with gomisins G and J, and not A. We found that gomisins G and J extracted from Schisandria chinensis can inhibit the P. gingivalis lipopolysaccharide induced-inflammatory responses in Raw264.7 cells.
[Show abstract][Hide abstract] ABSTRACT: The lipopolysaccharide (LPS) of Porphyromonas gingivalis is thought to induce periodontitis. In this study, we isolated Schisandrin from the dried fruits of Schisandra chinensis and examined the anti-inflammatory effect of Schisandrin in macrophages stimulated with LPS from P. gingivalis. First, Schisandrin inhibited LPS-induced pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. And Schisandrin suppressed the nuclear translocation and activity of NF-κB and phosphorylation of IκBα in LPS-stimulated RAW 264.7 cells. Next, the presence of a selective inhibitor of HO-1 (SnPP) and a siRNA specific for HO-1 inhibited Schisandrin-mediated anti-inflammatory activity. Furthermore, Schisandrin induced HO-1 expression of RAW 264.7 cells through Nrf-2, PI3K/Akt, and ERK activation. Therefore, these results suggest that the anti-inflammatory effects of Schisandrin on P. gingivalis LPS-stimulated RAW 264.7 cells may be due to a reduction of NF-κB activity and induction of the expression of HO-1, leading to TNF-α, IL-1β, and IL-6 down-regulation.
[Show abstract][Hide abstract] ABSTRACT: Garlic has garnered attention as a useful material which contains many bioactive molecules for the prevention and/or treatment
of various human ailments, including infectious diseases. In this study we tested several extracts of garlic on cellular activity
in human neutrophils. Stimulation of human neutrophils with chloroform extract of garlic (GCE) elicited intracellular calcium
([Ca2+]i) increases in a phospholipase C independent manner. GCE also stimulated superoxide anion production, which was completely
blocked by a calcium (Ca2+) chelator. We also observed that stimulation of human neutrophils with GCE caused production of the chemokine CXCL8 in a
concentration-dependent manner. GCE also stimulated activity of two important mitogen activated protein kinases (MAPKs), extracellular
signal-regulated kinase (ERK) and p38 MAPK. Moreover, GCE-induced CXCL8 production was inhibited by a p38 MAPK inhibitor (SB203580)
but not by an ERK inhibitor (PD98059). Taken together, our results demonstrate that GCE contains bioactive natural compounds
that stimulate [Ca2+]i signaling, superoxide anion production, and CXCL8 production. Thus, GCE may be useful for the development of immune-modulating
agents against infectious diseases.
[Show abstract][Hide abstract] ABSTRACT: A novel alpha-iso-cubebenol, which has anti-inflammatory effects in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages, was isolated from the fruits of Schisandra chinensis. alpha-iso-cubebenolinhibited LPS-induced nitric oxide (NO) and prostaglandin E(2) (PGE(2)) production. Consistent with these findings, alpha-iso-cubebenol also reduced the LPS-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 at the protein and mRNA levels in a concentration-dependent manner. alpha-iso-cubebenol also inhibited LPS-induced nuclear translocation of the NF-kappaB p65 subunit. Furthermore, alpha-iso-cubebenol suppressed the phosphorylation of ERK, JNK, and p38 kinase induced by LPS. Since the novel alpha-iso-cubebenol blocked the production of several pro-inflammatory mediators induced by LPS in macrophages, the molecule can be useful material for the development of anti-inflammatory agents against bacterial infections or endotoxin.
Biochemical and Biophysical Research Communications 01/2010; 391(4):1687-92. DOI:10.1016/j.bbrc.2009.12.131 · 2.30 Impact Factor