• 대한한의학방제학회지
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• 제10권2호
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• pp.189-197
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• 2002

The inhibitory effects of ethanol extract of Radex Angelica uchiyamana, on LPS- or IFN- plus LPS-induced production of NO, and $TNF-{\alpha}$, and expression of iNOS and COX-2 were investigated in the activated RAW 264.7 cells. This extract significantly inhibited the production of NO and $TNF-{\alpha}$, and suppressed the expression of iNOS and COX-2 in a dose-dependent manner. These results show that ethanol extract of Radex Angelica uchiyamana may explain some known biological activities including anti-inflammatory effect, and is of considerable benefit in the treatment for NO and pro-inflammatory cytokine overproduction related immunological diseases.

• Tuberculosis and Respiratory Diseases
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• 제71권2호
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• pp.97-105
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• 2011

Background: It was hypothesized that the immunomodulating effects of moxifloxacin contribute to ameliorate oleic acid (OA)-induced acute lung injury (ALI) by suppression of cytosolic phospholipase A2 (cPLA2). This was based on observations from experiments on rats associated with neutrophilic respiratory burst, cPLA2 activity, and expressions of cPLA2, $TNF{\alpha}$, and COX-II in the lung. Methods: ALI was induced by intravenous injection of OA in male Sprague-Dawley rats. Five hours after OA injection, protein content in bronchoalveolar lavage (BAL), lung myeloperoxidase (MPO) activity, and numbers of BAL neutrophils were measured. As an index of oxidative stress-induced lung injury, the content of malondialdehyde (MDA) in lung tissues was also determined. Lung histology, immunohistochemistry and determination of activity of cPLA2 in lung tissues were carried out. In addition, Western blotting of $TNF{\alpha}$ and COX-II in lung tissues was performed. Results: The accumulation of neutrophils in the lungs was observed after OA injection. BAL protein was increased along with neutrophilic infiltration and migration by OA. Moxifloxacin decreased all of these parameters of ALI and ameliorated ALI histologically. The increased malondialdehyde (MDA) in the lung by OA was also decreased by moxifloxacin. Moxifloxacin not only suppressed cPLA2 expression in the lungs and neutrophils but also decreased cPLA2 activity in lung tissues of rats given OA. The enhanced expressions of $TNF{\alpha}$ and COX-2 in the lung tissues of rats given OA were also suppressed by moxifloxacin. Conclusion: Moxifloxacin inhibited cPLA2 and down-regulated $TNF{\alpha}$ and COX-2 in the lungs of rats given OA, which resulted in the attenuation of inflammatory lung injury.

• 동의생리병리학회지
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• 제26권2호
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• pp.175-180
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• 2012

The purpose of this study is to verify the anti-inflammatory effectiveness of Cheongyeoungkeumyeum(CYK) including seven herbal medicines of that major effectiveness is to clear heat, to relieve fire toxicity and to clear damp-heat. To evaluate anti-inflammatory effectiveness of CYK, we measured the production of reactive oxygen species(ROS), nitric oxide(NO) cyclooxygenase-2(COX-2) and in TNF-${\alpha}$ LPS-activated Raw 264.7 cells. Cell viability was determined by MTT assay. The concentrations of ROS and relative level of NO were measured with DPPH assay and Griess reagent, respectively. COX-2 and TNF-${\alpha}$ were detected by enzyme immuno assay(EIA) and enzyme-linked immunosorbent assay(ELISA). As a result, we found that CYK suppressed LPS-induced ROS and NO production in a dose-dependent manner. Also CYK significantly inhibited LPS-induced COX-2 activity and the release of TNF-${\alpha}$. These results indicate that the CYK may have an anti-inflammatory agent for the treatment of various inflammatory disease.

• Biomolecules & Therapeutics
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• 제23권2호
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• pp.110-118
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• 2015

According to the expansion of lifespan, neuronal disorder based on inflammation has been social problem. Therefore, we isolated shikonin from Lithospermum erythrorhizon and evaluated anti-inflammatory effects of shikonin in lipopolysaccharide (LSP)-stimulated BV2 microglial cells. Shikonin dose-dependently inhibits the expression of the proinflammatory mediators, nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and tumor necrosis factor-${\kappa}B$ (TNF-${\alpha}$) as well as their main regulatory genes and products such as inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-${\alpha}$ in LPS-stimulated BV2 microglial cells. Additionally, shikonin suppressed the LPS-induced DNA-binding activity of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) to regulate the key regulatory genes of the proinflammatory mediators, such as iNOS, COX-2, and TNF-${\alpha}$, accompanied with downregulation of reactive oxygen species (ROS) generation. The results indicate that shikonin may downregulate the expression of proinflammatory genes involved in the synthesis of NO, $PGE_2$, and TNF-${\alpha}$ in LPS-treated BV2 microglial cells by suppressing ROS and NF-${\kappa}B$. Taken together, our results revealed that shikonin exerts downregulation of proinflammatory mediators by interference the ROS and NF-${\kappa}B$ signaling pathway.

• 생약학회지
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• 제41권1호
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• pp.14-20
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• 2010

In this study, we investigated the anti-inflammatory effects of fupenjic acid (FA) isolated from the Potentilla discolor in both RAW 264.7 and mouse primary peritoneal macrophage cells. FA pretreatment significantly inhibited nitric oxide (NO) and prostaglandin $E_2(PGE_2)$ productions in the lipopolysaccharide (LPS)-induced RAW 264.7 and mouse primary peritoneal macrophage cells. Consistent with these observations, Western blot and RT-PCR analyses revealed that FA inhibited the LPS-induced expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels. In addition, FA reduced the release of tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and interleukin-6 (IL-6). These results suggest that the down regulation of iNOS and COX-2 expression and TNF-$\alpha$ and IL-6 production by fupenjic acid are responsible for its anti-inflammatory effects.

• 생약학회지
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• 제39권2호
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• pp.95-103
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• 2008

In the present study, we investigated the anti-inflammatory effects by kaempferol-3-O-${\beta}$-D-sophoroside (KS) isolated from Sophora japonica (Leguminosae) on the lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin ($PGE_2$) production by RAW 264.7 cell line compared with kaempferol. KS significantly inhibited the LPS-induced NO and $PGE_2$ production. Consistent with these observations, KS reduced the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein and mRNA levels in a concentration-dependent manner. In addition, the release and the mRNA expression levels of tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) and interleukin-6 (IL-6) were also reduced by KS. Moreover, KS attenuated the LPS-induced activation of nuclear factor-kappa B ($NF{-\kappa}B$), a transcription factor necessary for pro-inflammatory mediators, iNOS, COX-2, $TNF-{\alpha}$ and IL-6 expression. These results suggest that the down regulation of iNOS, COX-2, $TNF-{\alpha}$, and IL-6 expression by KS are achieved by the downregulation of $NF{-\kappa}B$ activity, and that is also responsible for its anti-inflammatory effects.

• Journal of Ginseng Research
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• 제36권2호
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• pp.146-152
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• 2012

Panax ginseng (PG) is a globally utilized medicinal herb. The medicinal effects of PG are primarily attributable to ginsenosides located in the root and leaf. The leaves of PG are known to be rich in various bioactive ginsenosides, and the therapeutic effects of ginseng extract and ginsenosides have been associated with immunomodulatory and anti-inflammatory activities. We examined the effect of PG leaf extract and the isolated ginsenosides, on nuclear factor (NF)-${\kappa}B$transcriptional activity and target gene expression by applying a luciferase assay and reverse transcription polymerase chain reaction in tumor necrosis factor (TNF)-${\alpha}$-treated hepatocarcinoma HepG2 cells. Air-dried PG leaf extract inhibited TNF-${\alpha}$-induced NF-${\kappa}B$transcription activity and NF-${\kappa}B$-dependent cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) gene expression more efficiently than the steamed extract. Of the 10 ginsenosides isolated from PG leaves, Rd and Km most significantly inhibited activity in a dose-dependent manner, with $IC_{50}$ values of $12.05{\pm}0.82$ and $8.84{\pm}0.99\;{\mu}M$, respectively. Furthermore, the ginsenosides Rd and Km inhibited the TNF-${\alpha}$-induced expression levels of the COX-2 and iNOS gene in HepG2 cells. Air-dried leaf extracts and their chemical components, ginsenoside Rd and Km, are involved in the suppression of TNF-${\alpha}$-induced NF-${\kappa}B$ activation and NF-${\kappa}B$-dependent iNOS and COX-2 gene expression. Consequently, air-dried leaf extract from PG, and the purified ginsenosides, have therapeutic potential as anti-inflammatory.

• 대한본초학회지
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• 제34권1호
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• pp.51-57
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• 2019

Objectives : Nypa fruticans Wurmb. (NF) have been used as a traditional medicine to treat inflammatory diseases in East-South Asia. However, it is largely undiscovered whether NF water extract could exhibit anti-inflammatory activities against tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced inflammatory responses on human keratinocytes, HaCaT cells. Therefore, this study was aimed to investigate the anti-inflammatory activity of NF water extract on TNF-${\alpha}$-induced inflammatory responses in HaCaT cells. Methods : To investigate the anti-inflammatory activites of NF water extract in HaCaT cells, the inflammatory model of HaCaT cells was established under a suitable concentration (10 ng/ml) of human TNF-${\alpha}$ (hTNF-${\alpha}$). HaCaT keratinocyte cells were pre-treated with NF water extract for 1 h, and then stimulated with hTNF-${\alpha}$. Then, the cells were harvested to measure the inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and prostaglandin $E_2$ ($PGE_2$), and pro-inflammatory cytokine including TNF-${\alpha}$ and interleukin (IL)-6. In addition, we examined the inhibitory mechanisms of NF, mitogen activated protein kinases (MAPKs) and inhibitory kappa B alpha ($I{\kappa}-B{\alpha}$) Results : The treatment of NF inhibited the hTNF-${\alpha}$-induced elevation of iNOS, COX-2, and $PGE_2$ in HaCaT cells. In addition, NF treatment inhibited the hTNF-${\alpha}$-induced elevation of TNF-${\alpha}$ and IL-6. Furthermore, NF treatment inhibited the activation of MAPKs but not degradation of $I{\kappa}-B{\alpha}$. Conclusions : Taken together, our result suggest that treatment of NF could inhibit the hTNF-${\alpha}$-induced inflammatory responses via deactivation of MAPKs in HaCaT cells. This study could suggest that NF could be a beneficial agent to prevent skin damage or inflammation.

• 한방안이비인후피부과학회지
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• 제22권1호
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• pp.108-119
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• 2009

Objectives : This study was carried out to investigate the effects of Samhwangseje(SHSJ) on anti-Inflammation in Raw 264.7 cell. Methods : The effects of SHSJ on anti-Inflammation were measured by the cytotoxicity of Raw 264.7 cell, the inhibition for NO, TNF-$\alpha$, $PGE_{2}$, iNOS and COX-2, the blocking NF-${\kappa}B$ into nucleus. Results : 1. All concentrations of SHSJ had no cytotoxicity in Raw 264.7 cell. 2. All concentrations of SHSJ inhibited the production of NO in the Raw 264.7 cell stimulated with LPS. 3. All concentrations of SHSJ did not inhibit the production of TNF-$\alpha$ in the Raw 264.7 cell stimulated with LPS. 4. All concentrations of SHSJ inhibited the production of $PGE_{2}$ in the Raw 264.7 cell stimulated with LPS. 5. All concentrations of SHSJ did not inhibit the expression of COX-2 but concentrations of 50 ${\mu}g/ml$, 100 ${\mu}g/ml$ SHSJ inhibited iNOS expression in the Raw 264.7 cell stimulated with LPS. 6. Concentrations of 50 ${\mu}g/ml$, 100 ${\mu}g/ml$ SHSJ had the effect of blocking NF-${\kappa}B$ into nucleus in LPS-induced macrophage Raw 264.7 cell.

• 동의생리병리학회지
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• 제21권5호
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• pp.1154-1162
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• 2007

This study was to investigate the effects of Bee-venom Treatment on the monosodium iodoacetate(MIA)- induced osteoarthritis in rats. Arthritis was induced by injection of MIA(0.5 mg) into knee joints of rats. Arthritic rats were divided into control(n=8) and treated(n=8) group. Control group was injected with normal saline once a day for 20 days, while treated group was injected with Bee-venom extract once a day for same duration. Body weights were measured at 0, 5, 10, 15, 20 days after injection. At the end of experiment, gross and histopathological examination on the articular cartilages of the knee joints were performed. Proteoglycan contents of articular cartilages were analysed by safranine O staining method. The contents of $TNF-{\alpha}$, $IL-1{\beta}$ and IL-6 in synovial fluids were analysed by ELISA method. And also, COX-2 and iNOS immunohistochemical examination on the knee joints were performed. Body weights of the treated group were increased compared with control group at 20 days after injection. Grossly, the severity of osteoarthritis in the treated group were alleviated compared with control group. PG contents in articular cartilages of the treated group were significantly increased compared with control group. Histopathologically, degenerative and necrotic lesion of articular cartilages in the treated group were alleviated compared with those of the control group. $TNF-{\alpha}$ contents in synovial fluids of the treated group were decreased compared with control group. Positive reactions of COX-2 in chondrocytes and synovial membranes of the treated group were decreased compared with the control group. On the basis of these results, we concluded that Bee-venom treatment has anti-arthritic effects on the monosodium iodoacetate-induced osteoarthritis in rats. And it's effects were related with reduced secretion of $TNF-{\alpha}$ and COX-2 from osteoarthritic chondrocytes and synovial membranes.