• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.104-109
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• 2008

We previously reported that anti-inflammatory properties of poncirin, isolated from fruit of Poncirus trifoliata, might be the result from the inhibition of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis $factor-{\acute{a}}$ ($TNF-{\alpha}$) and interlukin-6 (IL-6) expression via the down-regulation of $NF{-\kappa}B$ binding activity. In this study, we investigated whether poncirin has an inhibitory effect on the production of pro-inflammatory mediators ex vivo and whether poncirin could relieve the symptoms of dextran sulfate sodium (DSS)-induced colitis in mice model of inflammatory bowel disease. Poncirin significantly inhibited the productions of NO, IL-6 and $TNF-{\alpha}$ in lipopolysaccharide (LPS)-induced mouse peritoneal macrophage. In addition, poncirin-treated mice when compared to control mice not receiving treatment recovered better from the weight loss caused by DSS-induced colitis. Changes in disease activity index (DAI) of poncirin-treated mice were also more favorable than for control mice and were comparable with mice treated with a typical anti-inflammatory-drug, 5-aminosalichylic acid (5-ASA). In addition, suppression of plasma NO and IL-6 productions of poncirin-treated mice was also observed in DSS-induced colitis. These results suggest that poncirin has potentially useful anti-inflammatory effects mediated by suppression of inflammatory mediator productions.

• Biomolecules & Therapeutics
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• v.21 no.3
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• pp.216-221
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• 2013

Aromadendrin, a flavonol, has been reported to possess a variety of pharmacological activities such as anti-inflammatory, antioxidant, and anti-diabetic properties. However, the underlying mechanism by which aromadendrin exerts its biological activity has not been extensively demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and $PGE_2$. In accordance, aromadendrin attenuated LPS-induced overexpression iNOS and COX-2. In addition, aromadendrin significantly suppressed LPS-induced degradation of $I{\kappa}B$, which sequesters NF-${\kappa}B$ in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF-${\kappa}B$. To elucidate the underlying signaling mechanism of anti-inflammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin significantly attenuated LPS-induced activation of JNK, but not ERK and p38, in a concentration-dependent manner. Taken together, the present study clearly demonstrates that aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-${\kappa}B$ and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.

• Preventive Nutrition and Food Science
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• v.21 no.3
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• pp.236-244
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• 2016

In this study, we compared the anti-inflammatory activity of Pinus koraiensis cone bark extracts prepared by conventional extraction and microwave-assisted extraction (MAE). Water extracts and 50% ethanol extracts prepared using MAE were applied to RAW 264.7 cell at 5, 10, 25, and $50{\mu}g/mL$ of concentrations, and tested for cytoxicity. The group treated with $50{\mu}g/mL$ of 50% ethanol extracts showed toxicity. In order to investigate the inhibition of nitric oxide (NO) production in RAW 264.7 cells, extracts of water and ethanol were treated with 5, 10, and $25{\mu}g/mL$ concentrations. The inhibitory activity of water and 50% ethanol extracts groups were determined as 40% and 60% at $25{\mu}g/mL$ concentration, respectively. We found concentration dependent decreases on inducible NO synthase. The inhibitory effect against forming inflammatory cytokines, prostaglandin $E_2$, tumor necrosis factor-${\alpha}$, interleukin (IL)-6, and IL-$1{\beta}$, was also superior in the $25{\mu}g/mL$ treated group than the control group. According to these results, the water extracts and 50% ethanol extracts both inhibited inflammatory mediators by reducing the inflammatory response. Therefore, The MAE extracts of P. koraiensis cone bark can be developed as a functional ingredient with anti-inflammatory activity.

• CELLMED
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• v.6 no.2
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• pp.13.1-13.7
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• 2016

Fatigue is a common complaint and affects the quality of life in modern people. Physical stress may induce activation of certain immune cells. Fermented porcine placenta (FPP) has been used to alleviate fatigue. Inflammatory cytokines are produced by physical stress and results in symptoms of fatigue. However, the role of FPP on fatigue-associated inflammatory cytokine production has not been elucidated yet. Thus, we estimated the anti-fatigue effect of FPP and its active components, leucine (Leu) and lysine (Lys) in activated RAW264.7 macrophages and forced swimming test (FST) fatigue animal model. Pretreatment with FPP, Leu, or Lys significantly inhibited the lipopolysaccharide (LPS)-induced tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 production without inducing cytotoxicity on LPS-stimulated RAW264.7 macrophages. FPP, Leu, or Lys inhibited the production of nitric oxide and downregulated the expression of inducible nitric oxide synthase on LPS-stimulated RAW264.7 macrophages. Furthermore, caspase-1 activities increased by LPS were significantly reduced by FPP, Leu, or Lys. In the FST, inflammatory cytokine levels of the mice administrated with FPP, Lys, and Leu were significantly reduced compared with the control group at 21 days. Collectively, these results show that anti-fatigue effect of FPP and its active components, Leu and Lys might be derived from the down-regulating of inflammatory mediators.

• Food Science of Animal Resources
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• v.34 no.6
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• pp.829-835
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• 2014

Inflammatory bowel disease (IBD) is caused by dysregulation of colon mucosal immunity and mucosal epithelial barrier function. Recent studies have reported that lipoteichoic acid (LTA) from Lactobacillus plantarum K8 reduces excessive production of pro-inflammatory cytokine. In this study, we investigated the preventive effects of lysate of Lb. plantarum K8 in dextran sulfate sodium (DSS)-induced colitis. Male Sprague-Dawley rats were orally pretreated with lysate of Lb. plantarum K8 (low dose or high dose) or live Lb. plantarum K8 prior to the induction of colitis using 4% DSS. Disease progression was monitored by assessment of disease activity index (DAI). Histological changes of colonic tissues were evaluated by hematoxylin and eosin (HE) staining. Tumor necrosis factor-alpha (TNF-${\alpha}$), interleukin-6 (IL-6) levels were measured using enzyme-linked immunosorbent assay (ELISA). The colon mRNA expressions of TNF-${\alpha}$, IL-6, and toll like receptor-2 (TLR-2) were examined by quantitative real-time-transcription polymerase chain reaction (qPCR). Lysate of Lb. plantarum K8 suppressed colon shortening, edema, mucosal damage, and the loss of DSS-induced crypts. The groups that received lysate of Lb. plantarum K8 exhibited significantly decreased levels of the pro-inflammatory cytokines TNF-${\alpha}$ and IL-6 in the colon. Interestingly, colonic expression of toll like receptor-2 mRNA in the high-dose lysate of Lb. plantarum K8 group increased significantly. Our study demonstrates the protective effects of oral lysate of Lb. plantarum K8 administration on DSS-induced colitis via the modulation of pro-inflammatory mediators of the mucosal immune system.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.6
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• pp.1320-1331
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• 2009

Oxidative stress and inflammation are important events in the development of chronic inflammatory diseases including arthritis, atherosclerosis, diabetes, hypertension. Cynomorium songaricum (CS) has been used as a traditional Korean herbal medicine, and it is currently used in traditional clinics to treat frequent urination, spermatorrhea, weakness of the sinews and constipation in the folk medicine. The aim of this study was to determine whether fractionated extracts of CS inhibit free radical generation such as DPPH radical, superoxide radical, nitric oxide and peroxynitrite, production of nitrite an index of NO, $PGE_2$, iNOS, COX-2 and pro-inflammatory cytokines in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages. Cytotoxic activity of extracts on RAW 264.7 cells was measured using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. Our results indicated that the most superior extract which scavenged DPPH radical, reactive oxygen species (ROS) and RNS was CS ethyl acetate extract (CSEA). Moreover, CSEA significantly inhibited the LPS-induced NO, $PGE_2$ production and iNOS, COX-2 expression accompanied by an attenuation of TNF-$\alpha$, IL-$1{\beta}$ and IL-6 formation in macrophages. Furthermore, CSEA treatment also blocked LPS-induced intracellular ROS production and the activation of NF-${\kappa}B$. These findings indicate that CSEA inhibits the production of pro-inflammatory mediators and cytokines via the suppression of ROS production and NF-${\kappa}B$ activation. Take together, these results indicate that CSEA has the potential for use as an natural anti-oxidant and an agent of anti-chronic inflammatory diseases.

• IMMUNE NETWORK
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• v.9 no.3
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• pp.98-105
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• 2009

Background: It has been recently noticed that type 2 diabetes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3'-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells. Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and followed by FACS analysis for the surface molecules. Results: Cordycepin inhibited the production of NO and pro-inflammatory cytokines such as IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ in LPS-activated macrophages via suppressing protein expression of pro-inflammatory mediators. T2D regulating genes such as $11{\beta}$-HSD1 and PPAR${\gamma}$ were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration. In accordance with suppressed pro-inflammatory cytokine production lead to inhibition of diabetic regulating genes in activated macrophages. Cordycepin suppressed NF-${\kappa}B$ activation in LPS-activated macrophages. Conclusion: Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-${\kappa}B$ dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

• The Journal of Korean Obstetrics and Gynecology
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• v.21 no.4
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• pp.69-89
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• 2008

Purpose: This study was performed to evaluate anti-oxidant activities and anti-inflammatory effects of Sungyoutanggagambang(SYTG). Methods: In the study of anti-oxidant activities. SYTG was investigated by DPPH radical scavenger activity. superoxide dismutase activity and superoxide anion radical scavenger activity. In the study of anti-inflammatory effects. SYTG was investigated using cultured cells and murine models. As for the parameters of inflammation. levels of several inflammatory cytokines and chemical mediators which are known to be related to inflammation were measured in mouse lung fibroblast cells(mLFCs) and RAW264.7 cells. Results: Prior to the experiment. we investigated the security of SYTG by measuring GOT and GPT in serum. 1. SYTG showed high antioxidant activity in a concentration-dependent degree by measured scavenging activity of DPPH free radical, superoxide dismutase and superoxide anion radical. 2. SYTG inhibited IL-1$\beta$, IL-6. TNF-$\alpha$, COX-2 and NOS-II mRNA expression as compared with the control group in a concentration-dependent degree in RAW264.7 cell line. 3. SYTG inhibited IL-1$\beta$, IL-6 production significantly at 100 ${\mu}g/ml$ and TNF-$\alpha$ production significantly at 50, 100 ${\mu}g/ml$ as compared with the control group in RA W264.7 cell line. 4. SYTG inhibited IL-1$\beta$, and IL-6 production significantly as compared with the control group in serum of acute inflammation-induced mice. and decreased IL-1$\beta$, IL-6 production in spleen tissue. and also decreased IL-1$\beta$, IL-6 production in liver tissue. Conclusion: These results suggest that SYTG can be useful in treating diverse female diseases caused by inflammation such as endometrosis, myoma, pelvic congestion. chronic cervicitis, chronic pelvic inflammatory disease and so on.

• The Journal of Korean Medicine
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• v.40 no.3
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• pp.35-58
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• 2019

Objectives: The aim of this study was to investigate the anti-inflammatory effects of Curcuma longa rhizoma extract in an experimental rat model of osteoarthritis. Methods: Osteoarthritis was induced in rats by injecting monosodium iodoacetate (MIA) into the knee joint cavity of rats. The rats were divided into 5 groups (Normal, Control, positive comparison, low (CL) and high (CH) concentration groups). Rats in the low concentration (CL) group had MIA-induced osteoarthritis; they were treated with Curcuma longa rhizoma extract at a dose of 50mg/kg body weight. Rats in the high concentration (CH) group had MIA-induced osteoarthritis; they were treated with Curcuma longa rhizoma extract at a dose of 100mg/kg body weight. Hind paw weight distribution and ROS levels were measured. At the end of all treatments, changes in alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and creatinine levels were analyzed. In addition, inflammatory protein levels were evaluated by western blot analysis. Results: In this study, hind paw weight distribution significantly improved in the CL and CH groups, while. Reactive oxygen species (ROS) production significantly decreased in both. The levels of ALT, AST, BUN, and creatinine did not significantly change in either group. The production of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), $p47^{phox}$, and Ras-related C3 botulinum toxin substrate 1 (RAC1) decreased in both. Catalase, heme oxygenase-1 (HO-1) and superoxide dismutase (SOD) significantly increased in the CL and CH groups, respectively. Nuclear factor erythroid 2 (Nrf2) increased, but there were no significant differences between the experimental and control groups. Inflammatory cytokines, including nuclear factor-kappa Bp65 (NF-${\kappa}Bp65$), interleukin-1beta (IL-$1{\beta}$), and tumor necrosis factor-alpha (TNF-${\alpha}$), decreased significantly in both the CL and CH groups. Conclusions: Our results showed that Curcuma longa rhizoma extract has anti-inflammatory effects. Anti-inflammatory activity is regulated by the inhibition of inflammatory cytokines and mediators, such as NF-${\kappa}B$, therefore, it suppresses cartilage damage as well.

• Journal of Microbiology and Biotechnology
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• v.32 no.1
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• pp.81-90
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• 2022

Peucedanum japonicum Thunberg (PJT) has been used in traditional medicine to treat colds, coughs, fevers, and other inflammatory diseases. The goal of this study was to investigate whether 3'-isovaleryl-4'-senecioylkhellactone (IVSK) from PJT has anti-inflammatory effects on lung epithelial cells. The anti-inflammatory effects of IVSK were evaluated using phorbol 12-myristate 13-acetate (PMA)-stimulated A549 cells and regular human lung epithelial cells as a reference. IVSK reduced the secretion of the inflammatory mediators interleukin (IL)-8 and monocyte chemoattractant protein-1 (MCP-1), and the mRNA expression of IL-6, IL-8, MCP-1, and IL-1β. Additionally, it inhibited the phosphorylation of IκB kinase (IKK), p65, Iκ-Bα, and mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK in A549 cells stimulated with PMA. Moreover, the binding affinity of activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) was significantly reduced in the luciferase assay, while nuclear translocation was markedly inhibited by IVSK in the immunocytochemistry. These findings indicate that IVSK can protect against inflammation through the AP-1 and NF-κB pathway and could possibly be used as a lead compound for the treatment of inflammatory lung diseases.