• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.200-206
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• 2014

N-(p-Coumaryol) tryptamine (CT), a phenolic amide, has been reported to exhibit anti-oxidant and anti-inflammatory activities. However, the underlying mechanism by which CT exerts its pharmacological properties has not been clearly demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of CT in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells. CT significantly inhibited LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and $PGE_2$, and protein expressions of iNOS and COX-2. In addition, CT significantly suppressed LPS-induced secretion of pro-inflammatory cytokines such as TNF-${\alpha}$ and IL-$1{\beta}$. To elucidate the underlying anti-inflammatory mechanism of CT, involvement of MAPK and Akt signaling pathways was examined. CT significantly attenuated LPS-induced activation of JNK/c-Jun, but not ERK and p38, in a concentration-dependent manner. Interestingly, CT appeared to suppress LPS-induced Akt phosphorylation. However, JNK inhibition, but not Akt inhibition, resulted in the suppression of LPS-induced responses, suggesting that JNK/c-Jun signaling pathway significantly contributes to LPS-induced inflammatory responses and that LPS-induced Akt phosphorylation might be a compensatory response to a stress condition. Taken together, the present study clearly demonstrates CT exerts anti-inflammatory activity through the suppression of JNK/c-Jun signaling pathway in LPS-challenged RAW264.7 macrophage cells.

• Korean Journal of Acupuncture
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• v.26 no.3
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• pp.43-54
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• 2009

Objectives : To investigate the anti-inflammatory effects of Prunella vulgaris pharmacopuncture in lipopolysaccharide (LPS)-induced inflammatory rat model. Methods : Sprague-Dawley rats were divided into 5 groups; normal control (n=8), LPS control (n=8), LPS+Prunella vulgaris pharmacopuncture at CV4 (CV4, n=8), LPS+Prunella vulgaris pharmacopuncture at ST36 (ST36, n=8), and LPS+Prunella vulgaris pharmacopuncture at CV12 (CV12, n=8). Pharmacopuncture was given every two days for 4 weeks followed by inflammation induction by peritoneal LPS injection (5mg/kg). Proinflammatory cytokines including interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6), tumor necrosis factor-$\alpha$ (TNF-$\alpha$), interleukin-10 (IL-10), thiobarbituric acid reactive substance (TBARS) from blood and liver tissue were compared before and 5 hrs after inflammation induction. Results : In CV4 and CV12 groups, plasma IL-$1{\beta}$, IL-6 and TNF-$\alpha$ levels increased by LPS injection, significantly decreased 5 hrs after injection (p<0.05). For CV12 group, plasma IL-10 concentration significantly increased (p<0.05). Liver IL-$1{\beta}$ and IL-6 levles significantly decreased in CV4 and CV12 groups (P<0.05), while normal and LPS control groups were not significantly different in TNF-$\alpha$ and IL-10 levels. Plasma TBARS concentration was significantly decreased in CV12 group, while there was no significant difference among LPS control and pharmacopuncture groups for liver TBARS concentration. Conclusions : Based on the present findings, Prunella vulgaris pharmacopuncture at CV12 may have a potentially preventive anti-inflammatory effect in an LPS-induced inflammatory rat model.

• Journal of Acupuncture Research
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• v.30 no.3
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• pp.61-73
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• 2013

Objectives : This study was designed to evaluate the effects of Phaseoli Semen Herbal-acupuncture(PS-HA) at $KI_{10}$ in acute nephritis induced by lipopolysaccharide(LPS) in rat. Methods : The rats were divided into 5 groups, which were control, LPS, PS-HA, NP and saline group. LPS, PS-HA, NP and saline groups were given LPS to induce acute nephritis and control group did not receive LPS. LPS group did not receive any treatment after the onset of acute nephritis. PS-HA, NP and saline group received PS-HA, normal acupuncture, and saline injection at $KI_{10}$ three times per week, respectively. To evaluate the effect of PS-HA at $KI_{10}$, the complete blood count, BUN, creatinine, TNF-${\alpha}$, and CINC-1 in serum were measured. To show its effect on renal function, creatinine, and total protein in urine was measured as well as urine output. The level of myeloperoxidase in renal tissue was quantified and complete histology was done in kidney samples obtained from the rats. Results : PS-HA group showed a significant reduction in the proportion of WBC and neutrophil, serum BUN, TNF-${\alpha}$, and CINC-1 compared to LPS group. Furthermore, a significant increase in urine output and a decrease in urinary creatinine level, MPO in renal tissue, and number of neutrophils at glomerulus was observed in PS-HA group compared to LPS group Conclusions : PS-HA at $KI_{10}$ was shown to have a significantly effect on treating LPS induced acute nephrits. Therefore, future study is needed to further evaluate the clinical usefulness of PS-HA at $KI_{10}$ in treating acute nephritis.

• International Journal of Oral Biology
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• v.33 no.4
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• pp.149-154
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• 2008

Porphyromonas gingivalis, a major periodontal pathogen, has been implicated in the initiation and progression of periodontal disease. Endothelial dysfunction (Editor note: Aberrant and dysfunction are somewhat redundant. The authors may want to choose one or the other.) contributes to chronic periodontal inflammation. Using cDNA-representational difference analysis, we found that P.gingivalis lipopolysaccharide differentially induces a number of genes in human microvascular endothelial cells. Among these upregulated genes, we focused on intercellular adhesion molecule-1 (VCAM-1), which is crucial for leukocyte recruitment during vascular inflammation. P. gingivalis LPS significantly increased the expression of vascular cell adhesion molecule-1 (VCAM-1) as well as ICAM-1. Promoter assays revealed that the transcription of these cell adhesion molecules was mainly regulated by nuclear factor-${\kappa}B$ (NF-${\kappa}B$) in endothelial cells. Furthermore, P. gingivalis LPS significantly increased leukocyte adhesiveness to microvascular endothelial cells and to aortic endothelium. Taken together, our results demonstrate that P. gingivalis LPS activates microvascular endothelial cells through NF-${\kappa}B$-dependent expression of cell adhesion molecules.

• Journal of Korean society of Dental Hygiene
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• v.18 no.4
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• pp.423-432
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• 2018

Objectives: Calcium hydroxide, a root canal temporary sealer, has long been used and it has anti-bacterial and anti-inflammatory activity. To investigate the properties of a newly developed calcium hydroxide paste comprising silicon-substituted hydroxyapatite (Si-HA), we examined the anti-inflammatory activity of the new calcium hydroxide paste in RAW 264.7 macrophages stimulated by lipopolysaccharide (LPS), which causes infection of the root canal. Methods: The test materials, including Calcipex II as control group and the newly developed TRC paste, were extracted from cell culture media and then diluted for experiment. In LPS-stimulated RAW 264.7 cells, the cytotoxicity and nitric oxide (NO) production of test materials were measured by MTT assay and Griess reagents, respectively. Also, the expression of the inducible nitric oxide synthase (iNOS) was assessed by western blotting. Results: The IC50 values of Calcipex II and TRC paste were $17.6mg/m{\ell}$ and $13.5mg/m{\ell}$, respectively. The level of NO, increased by LPS, was dose-dependently inhibited more by TRC paste than Calcipex II treatment. In addition, iNOS expression was decreased by 71% and 92% at concentrations of $2mg/m{\ell}$ and $20mg/m{\ell}$ of TRC paste, respectively. Conclusions: We demonstrated that the Si-HA calcium hydroxide paste has a slightly improved anti-inflammatory property and further studies are needed before clinical recommendations are proposed.

• The Korea Journal of Herbology
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• v.21 no.2
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• pp.165-173
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• 2006

Objectives : Coptidis Rhizoma has been known traditional medicine with antimicrobial activities. We investigated inhibitory effects of Coptidis Rhizoma extract on lipopolysaccharide(LPS)-induced nitric oxide production from mouse macrophages. Methods : After Coptidis Rhizoma extract was pretreated in BV2, mouse brain macrophages and RAW264.7 mouse macrophages, cells were activated with LPS. To investigate cytotoxicity Coptidis Rhizoma extract, cell viability was measured by MTT assay. The production of nitric oxide(NO) and inducible nitric oxide synthase(iNOS) was determined in each culture supernatant and mRNA by Griess reaction and RT-PCR. The production of $TNF-{\alpha}$ from cells was measured by ELISA. Results : Coptidis Rhizoma extract significantly inhibited LPS-induced NO production in BV2 and RAW264.7 cells. Coptidis Rhizoma extract also greatly suppressed mRNA expression of iNOS in BV2 and RAW264.7 cells activated by LPS. Conclusion : These data suggests that Coptidis Rhizoma extract may have an anti-inflammatory effect through the inhibition of NO production.

• Herbal Formula Science
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• v.16 no.2
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• pp.219-228
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• 2008

Objective : The present study was designed to investigate whether the water extract of the root of Scutellaria baicalensis could regulate lipopolysaccharide (LPS)-induced type 1 interferon. Methods : To evaluate of type 1 interferon inhibitory effect of the root of Scutellaria baicalensis, we examined type 1 interferon in LPS-stimulated RAW264.7 cells. Furthermore, Interleukin (IL)-10 and interferon regulatory factor (IRF) - 1, 7 expression level were examined to study the inhibition mechanisms. Results 1. Extract from the root of Scutellaria baicalensis didn't have any cytotoxity itelf. 2. Extract from the root of Scutellaria baicalensis inhibited interferon-a,b in dose dependant- and type 1 interferon production in time dependant manner. 3. Extract from the root of Scutellaria baicalensis reduced IL-10 and IRF-1, 7 production in LPS-stimulated RAW 264.7 cells. Conclusion : The extract from the root of Scutellaria baicalensis down-regulated LPS-induced type 1 interferon through suppression of IL-10 and IRF-1, 7 expression. This results suggested that the extract from the root of Scutellaria baicalensis may be a beneficial drug against inflammatory diseases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.3
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• pp.410-415
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• 2010

The purpose of this study was to investigate the anti-inflammatory effects of aqueous extract from Belamcanda chinensis (BC) on the RAW 264.7 cells. To evaluate the anti-inflammatory effects of BC, we examined the cytokine productions including nitric oxide (NO), interleukin (IL)-1b, IL-6 and tumor necrosis factor-a (TNF-a) in lipopolysaccharide (LPS)-induced RAW 264.7 cells and also inhibitory mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-kB) using Western blot. BC inhibited LPS-induced production of NO, IL-6 and TNF-a but not of IL-1b in RAW 264.7 cells. BC respectively inhibited the activation of MAPKs such as c-Jun NH2-terminal kinase (JNK) and p38 but not of extracelluar signal-regulated kinase (ERK 1/2) and NF-kB in the LPS-stimulated RAW 264.7 cells. Taken together, Our results showed that BC down-regulated LPS-induced NO, IL-6 and TNF-a productions mainly through JNK and p38 MAPK pathway.

• Food Science of Animal Resources
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• v.43 no.5
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• pp.938-947
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• 2023

In the present study, we aimed to examine the inhibition of genomic DNA from Lactiplantibacillus plantarum (LpDNA) on Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammatory responses in RAW264.7 cells. Pretreatment with LpDNA for 15 h significantly inhibited PgLPS-induced mRNA expression and protein secretion of interleukin (IL)-1β, IL-6, and monocyte chemoattractant protein-1. LpDNA pretreatment also reduced the mRNA expression of Toll-like receptor (TLR)2 and TLR4. Furthermore, LpDNA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and the activation of nuclear factor-κB (NF-κB) induced by PgLPS. Taken together, these findings demonstrate that LpDNA attenuates PgLPS-induced inflammatory responses by regulating MAPKs and NF-κB signaling pathways through the suppression of TLR2 and TLR4 expression.

• Toxicological Research
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• v.23 no.4
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• pp.289-299
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• 2007

Lipopolysaccharide (LPS) endotoxin is an active component in the outer membrane of Gram-negative bacteria. LPS is usually used as an inflammatory animal model. During the inflammation, diarrhea and changes in plasma proteins, in hepatic and/or intestinal microsomal cytochrome P450 (CYP) isozymes, and in the renal and/or biliary excretion of drugs have been reported. Thus, in rats pretreated with lipopolysaccharide endotoxin isolated from Klebsiella pneumoniae (KPLPS rats), the absorption, distribution, metabolism, and excretion of drugs could be expected to be altered. Interestingly time-dependent effects on the hepatic CYP isozymes have been reported in KPLPS rats. Thus, in KPLPS rats, the pharmacokinetics of drugs which are mainly metabolized via CYP isozymes could be expected to be time-dependent. In this review, an attempt to explain changes in pharmacokinetics of drug reported in the literature was made in terms of CYP isozyme changes or urinary and/or biliary excretion changes in KPLPS rats.