• CELLMED
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• v.13 no.6
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• pp.7.1-7.6
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• 2023

Raphanus sativus L. has been reported to have anti-inflammatory and anti-tumor activity. However, the anti-inflammatory effect and mechanism of action of the Raphanus sativus L. seeds (RSS) with or without oil are still unknown. This study was undertaken to investigate the in-vitro anti-inflammatory effect with or without oil in the RSS on RAW 264.7 cells stimulated by lipopolysaccharide (LPS). Results showed the suppressed LPS-induced secretion of pro-inflammatory mediators such as nitric oxide (NO), inflammatory cytokine (IL-6, TNF-α). Additionally, a decrease in protein expression of iNOS was observed, but nuclear translocation of NF-κB p65 was not inhibited. To elucidate the underlying mechanism of the anti-inflammatory effect of RSS, the involvement of mitogen-activated protein kinase (MAPK) signaling pathways was examined. We also found that RSS blocked LPS-induced phosphorylation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK) signaling but did not affect the phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK) 1/2. These results suggest that RSS may have potential as an anti-inflammatory agent through the inhibition of LPS-induced inflammatory cytokine production via regulation of the JNK pathway.

• Korean Journal of Medicinal Crop Science
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• v.17 no.2
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• pp.109-114
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• 2009

Rhubarb is the well-known and frequently used herbal medicine for the treatment of constipation, inflammation, and cancer. As described in the Korea and Chinese Pharmacopoeia, rhubarb consists of the roots and rhizomes of Rheum palmatum, R. officinale, and R. tanguticum. However, the pharmacological differences among rhubarb have not been scientifically established. In the present study, we investigated and compared the inhibitory effects of 70% ethanolic extracts from R. palmatum (RPE), R. officinale (ROE), R. nobile (RNE), and R. franzenbachii (RFE) on the production of inflammatory mediators, nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), interlukin-1beta ($IL-1{\beta}$), and tumor necrosis factor-alpha ($TNF-{\alpha}$) in RAW 264.7 macrophage cells. ROE, RNE, and RFE significantly inhibited the release of NO, $PGE_2$, $IL-1{\beta}$, and $TNF-{\alpha}$. RPE significantly reduced the release of $IL-1{\beta}$, but not NO, $PGE_2$, and $TNF-{\alpha}$. Overall, RFE was found to inhibit the release of $PGE_2$ and $IL-1{\beta}$, to a far greater degree than RPE, ROE, and RNE. Our results indicate that RFE possess the strongest anti-inflammatory activity among 4 tested rhubarb.

• International Journal of Oral Biology
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• v.31 no.3
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• pp.87-92
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• 2006

Schwann cells play an important role in peripheral nerve regeneration. Upon nerve injury, Schwann cells are activated and produce various proinflammatory mediators including IL-6, LIF and MCP-1, which result in the recruitment of macrophages and phagocytosis of myelin debris. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that necrotic cells induce immune cell activation via toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. To explore the possibility, we stimulated iSC, a rat Schwann cell line, with damaged neuronal cell extracts (DNCE). The stimulation of iSC with DNCE induced the expression of various inflammatory mediators including IL-6, LIF, MCP-1 and iNOS. Studies on the signaling pathway indicate that $NF-{\kappa}B$, p38 and JNK activation are required for the DNCE-induced inflammatory gene expression. Furthermore, treatment of either anti-TLR3 neutralizing antibody or ribonuclease inhibited the DNCE-induced proinflammatory gene expression in iSC. In summary, these results suggest that damaged neuronal cells induce inflammatory Schwann cell activation via TLR3, which might be involved in the Wallerian degeneration after a peripheral nerve injury.

• Biomolecules & Therapeutics
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• v.16 no.3
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• pp.277-285
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• 2008

Panax ginseng C.A. Mayer (Araliaceae, P. ginseng) has been used for the enhancement of vascular and immune functions in Korea and Japan for a long time. Ginsenoside $Rb_1$ and $Rg_3$ isolated from P. ginseng head-part butanolic extract (PGHB) were investigated for anti-inflammatory activity. Ginsenosides and PGHB did not affect the cell viability within $0\;-\;100\;{\mu}g/ml$ concentration to RAW 264.7 murine macrophage cells. Ginsenosides and PGHB inhibited partly lipopolysaccharide (LPS)-induced nitrite production in a dose-dependent manner. The ginsenosides and PGHB showed partially chemical nitric oxide (NO) quenching (maximum 40%) in the cell-free system. Also, ginsenoside $Rb_1$ and $Rg_3$ inhibited markedly approximately 74 and 54% of inducible nitric oxide synthase (iNOS) mRNA transcription from LPS-induced RAW 264.7 cells. Taken together, the inhibitory effect of ginsenosides and PGHB on NO production did not occur as a result of cell viability, but was caused by both the chemical NO quenching and the regulation of iNOS. Additionally, the ginsenoside $Rb_1$ and PGHB inhibited prostaglandin $E_2$ ($PGE_2$) synthesis in a concentration-dependent manner, showed approximately 70-98% inhibition at $100\;{\mu}g/ml$ concentration. And the treatment with ginsenosides and PGHB attenuated partially LPS-upregulated cyclooxygenase-2 (COX-2) gene transcription. Ginsenoside $Rg_3$ suppressed LPS-stimulated interleukin-6 (IL-6) level to the basal in RAW 264.7 cells. From these results, ginsenoside $Rb_1,\;Rg_3$, and PGHB may be useful for the relief and retardation of immunological inflammatory responses and its action may occur through the reduction of inflammatory mediators, including NO, $PGE_2$, and IL-6 production.

• Biomolecules & Therapeutics
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• v.23 no.6
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• pp.531-538
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• 2015

Preceding infection or inflammation such as bacterial meningitis has been associated with poor outcomes after stroke. Previously, we reported that intracorpus callosum microinjection of lipopolysaccharides (LPS) strongly accelerated the ischemia/reperfusionevoked brain tissue damage via recruiting inflammatory cells into the ischemic lesion. Simvastatin, 3-hydroxy-3-methylgultaryl (HMG)-CoA reductase inhibitor, has been shown to reduce inflammatory responses in vascular diseases. Thus, we investigated whether simvastatin could reduce the LPS-accelerated ischemic injury. Simvastatin (20 mg/kg) was orally administered to rats prior to cerebral ischemic insults (4 times at 72, 48, 25, and 1-h pre-ischemia). LPS was microinjected into rat corpus callosum 1 day before the ischemic injury. Treatment of simvastatin reduced the LPS-accelerated infarct size by 73%, and decreased the ischemia/reperfusion-induced expressions of pro-inflammatory mediators such as iNOS, COX-2 and IL-$1{\beta}$ in LPS-injected rat brains. However, simvastatin did not reduce the infiltration of microglial/macrophageal cells into the LPS-pretreated brain lesion. In vitro migration assay also showed that simvastatin did not inhibit the monocyte chemoattractant protein-1-evoked migration of microglial/macrophageal cells. Instead, simvastatin inhibited the nuclear translocation of NF-${\kappa}B$, a key signaling event in expressions of various proinflammatory mediators, by decreasing the degradation of $I{\kappa}B$. The present results indicate that simvastatin may be beneficial particularly to the accelerated cerebral ischemic injury under inflammatory or infectious conditions.

• The Journal of Korean Medicine
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• v.39 no.1
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• pp.63-74
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• 2018

Objectives: Periodontitis is an inflammatory disease with the destruction of periodontal ligament, alveolar bone loss and inflammation of gingva, leading to teeth loss. Eclipta prostrata L. (Ecliptae Herba) has been used to treat the inflammatory disease as a Korean traditional medicine. The aim of this study is to investigate the effects of E. prostrata L. on periodontitis. Methods: E. prostrata L. was extracted with water and lyophilized. The aqueous extract of E. prostrata L. (EP) was topically applied to the periodontal lesion for 2 weeks. To induce the periodontitis, a 3-0 nylon ligature was placed around the cervix of the lower first molar in rat. Rats were divided into 3 groups (n = 7); NL group (non-ligatured and non-treated), L group (ligatured and vehicle-treated) and EP group (ligatured and EP-treated). After sacrifice, the mandibles was dissected and stained with methylene blue solution to analyze the alveolar bone loss. The expression of MMP-9 was determined in gingival tissues. To confirm the effect of EP on recovery of gingiva, mRNA expressions of type I pro-collagen and MMP-9 levels were investigated in LPS-treated HS68 fibroblast cells. In addition, inflammatory mediators were evaluated in LPS-treated RAW264.7 cells. Results: Alveolar bone loss was significantly inhibited by EP treatment. The mRNA expression of MMP-9 was attenuated in rats treated with EP. In addition, treatment with EP increased the expression of type I pro-collagen, while the expression of MMP-9 was decreased in LPS-stimulated HS68 fibroblast cells. Furthermore, EP down-regulated the LPS-induced IL-6, $TNF-{\alpha}$, COX-2 and iNOS production in RAW264.7 cells. Conclusions: These results suggest that EP have ameliorative effects on periodontitis through inhibiting alveolar bone loss and modulating the inflammatory mediators. Therefore, E. prostrata L. may be an alternative on patients with periodontitis.

• Journal of Korean Medicine Rehabilitation
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• v.26 no.3
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• pp.1-15
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• 2016

Objectives This study was designed to evaluate the anti-inflammatory effects of Seungseup-tang (SST) on the monosodium iodoacetate (MIA)-induced osteoarthritis rats. Methods Osteoarthritis was induced by injection of MIA ($50{\mu}l$ with 80 mg/ml) into knee joint cavity of rats. Rats were divided into 4 groups (normal group, control group, indomethacin treated group, SST treated group, each n=6). Normal group was not injected with MIA and taken normal diet. Control group was injected with MIA and taken with distilled water. Indomethacin treated group was injected with MIA and taken indomethacin 5 mg/kg by oral administration. SST treated group was injected with MIA and taken SST 200 mg/kg by oral administration. We examined the weight-bearing ability of hind paw, biomarkers related to oxidative stress in serum, inflammatory proteins and inflammatory mediators and cytokines. Moreover, histopathological examination of knee joint structure was also performed by Hematoxylin & Eosin (H&E), Safranin-O staining method. Results In the present study, SST treated group showed a similar inhibitory effects alike indomethacin treated group, in most of the studied parameters of inflammation. The increased oxidative stress biomarker such as reactive oxygen species (ROS) and peroxy nitrite ($ONOO^-$) in the serum were reduced with SST. Especially, the level of $ONOO^-$ compared with control group significantly suppressed. Also, the expression of inflammatory mediators and cytokines induced by nuclear factor-kappa B (NF-${\kappa}B$) activation was modulated through inhibition of IkBa phosphorlation. In addition, histological analysis revealed that cartilage damage by MIA repaired markedly in SST treated group. Conclusions According to the results, Seungseup-tang may be effective for preventing the progression of osteoarthritis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.33 no.2
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• pp.116-122
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• 2019

The aim of this study is to evaluate the anti-inflammatory effect of Hataedock treatment using Coptidis Rhizome and Glycyrrhiza Uralensis (CG) mixed extract in allergic rhinitis induced NC/Nga mice. We divided NC/Nga mice into 3 groups as follows; allergic rhinitis-induced group after CG Hataedock treatment (CGT, n=10), no treatment group (Ctrl), allergic rhinitis elicited group (ARE). To induce allergic rhinitis, NC/Nga mice of 3 weeks age were sensitized on 7, 8 and 9week by Ovalbumin (OVA) antigen in intranasal space. Hataedock using CG extract was administered on week 3 in allergic rhinitis-induced group (CGT) after Hataedock treatment. To identify distribution of Interlukin (IL)-4, Cluster of differentiation 40 (CD40), high-affinity IgE receptor ($Fc{\varepsilon}RI$), substance P, Matrix metallopeptidase 9 (MMP-9), Nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) p65, Inducible nitric oxide synthase (iNOS) and Cycloxygenase-2 (COX-2), we used histological examination. CGT significantly inhibited IL-4 and CD40 response compared with ARE. The reduction of Th2 cytokine expression decreased inflammatory mediators such as $Fc{\varepsilon}RI$, substance P, MMP-9, $NF-{\kappa}B$ p65, iNOS and COX-2. Such immunological improvement induced reduction of respiratory epithelial damage and mucin secretion in goblet cell. These results indicate that Hataedock treatment suppresses allergic rhinitis through modulating of Th2 responses and diminishing various inflammatory mediators in nasal mucosal tissue. It might have potential applications for prevention and treatment of allergic rhinitis.

• Journal of Ginseng Research
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• v.45 no.4
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• pp.510-518
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• 2021

Background: Gintonin is a newly derived glycolipoprotein from the roots of ginseng. The purpose of this study is to investigate the anti-arthritic efficacy of Gintonin on various proteases and inflammatory mediators that have an important role in arthritis. Methods: Fibroblast-like synoviocytes (FLS) were treated with Gintonin and stimulated with interleukin (IL)-1β 1 hour later. The antioxidant effect of Gintonin was measured using MitoSOX and H₂DCFDA experiments. The anti-arthritic efficacy of Gintonin was examined by analyzing the expression levels of inflammatory mediators using RT-PCR, western blot, and ELISA. The phosphorylation of mitogen-activated protein kinase (MAPK) pathways and translocation of nuclear factor kappa B (NF-κB)/p65 into the nucleus were also analyzed using western blot, ELISA, and immunocytochemistry. Collagen-induced arthritis (CIA) mice model was used. Mice were orally administered with Gintonin (25, 50, and 100 mg/kg) every 2 days for 45 days. The body weight, arthritis score, squeaking score, and paw volume were measured as the behavioral parameters. After sacrifice, H&E and safranin-O staining were performed for histological analysis. Results: Gintonin significantly inhibited the expression of inflammatory intermediates. Gintonin prevented NF-κB/p65 from moving into the nucleus through the JNK and ERK MAPK phosphorylation in FLS cells. Moreover, Gintonin suppressed the symptoms of arthritis in the CIA mice model. Conclusion: As a result, the antioxidant and anti-inflammatory effects of Gintonin were demonstrated, and ultimately the anti-arthritic effect was proved. Collectively, Gintonin has a great potential as a therapeutic agent for arthritis treatment.

• The Korea Journal of Herbology
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• v.32 no.3
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• pp.1-7
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• 2017

Objective : The purpose of this study was to investigate the effects of Scrophulariae Radix Water Extract (SR) on the production of inflammatory mediators in RAW 264.7 mouse macrophages cells induced by lipopolysaccharide (LPS). Method : We examined effect of Scrophulariae Radix Extract on the cell viability of mouse macrophages cells. Futhermore, After 24 hours treatment we investigated anti-inflammatory effect of Scrophulariae Radix Extract by the production of Bio-Plex cytokine assay, concentrations of various cytokines such NO, $interleukin(IL)-1{\alpha}$, IL-3 and interferon inducible protein-10(IP-10). Result : No significant changes have been found in the mouse macrophge cell viability by the Scrophulariae Radix Extract at the concentration of 25, 50, 100 and $200{\mu}g/m{\ell}$. The water extract of Scrophulariae Radix significantly inhibited the production of NO in the LPS-induced macrophage at the concentration of 25, 50, 100 and $200{\mu}g/m{\ell}$. The water extract of Scrophulariae Radix significantly inhibited the production of $IL-1{\alpha}$, IL-3 and IP-10 in the LPS-induced macrophage at the concentration of 50, 100 and $200{\mu}g/m{\ell}$. Conclusion : The water extract of Scrophulariae Radix significantly inhibited the production of NO, $IL-1{\alpha}$, IL-3 and IP-10 at the concentration of $50{\mu}g/m{\ell}$ or higher in the LPS-induced macrophages with no changes in the cell viability of them. These results suggest that water extract of Scrophulariae Radix has anti-inflammatory effect related with its inhibition of proinflammatory cytokines such as $IL-1{\alpha}$, IL-3 and IP-10 in the LPS-induced macrophages.