In Situ Spray Polymerization of Conductive Polymers for Personalized E-textiles.

E-textiles, also known as electronic textiles, seamlessly merge wearable technology with fabrics, offering comfort and unobtrusiveness and establishing a crucial role in health monitoring systems. In this field, the integration of custom sensor designs with conductive polymers into various fabric types, especially in large areas, has presented significant challenges. Here, we present an innovative additive patterning method that utilizes a dual-regime spray system, eliminating the need for masks and allowing for the programmable inscription of sensor arrays onto consumer textiles. Unlike traditional spray techniques, this approach enables in situ, on-the-fly polymerization of conductive polymers, enabling intricate designs with submillimeter resolution across fabric areas spanning several meters. Moreover, it addresses the nozzle clogging issues commonly encountered in such applications. The resulting e-textiles preserve essential fabric characteristics such as breathability, wearability, and washability while delivering exceptional sensing performance. A comprehensive investigation, combining experimental, computational, and theoretical approaches, was conducted to examine the critical factors influencing the operation of the dual-regime spraying system and its role in e-textile fabrication. These findings provide a flexible solution for producing e-textiles on consumer fabric items and hold significant implications for a diverse range of wearable sensing applications.

Chondroprotective Effects of Ulva prolifera on Osteoarthritis through MAPKs Signaling Inhibition.

Osteoarthritis (OA) is a typical degenerative disease that mainly appears in the elderly aged 65 and over. OA is characterized by inflammation and decomposition of the cartilage matrix due to irreversible wear and tear. Ulva prolifera, a green macroalgae species, contains polysaccharides, amino acids, polyunsaturated fatty acids, and polyphenols, which are major active components responsible for anti-inflammatory and antioxidant effects. This study evaluated the chondro-protective effect of 30% prethanol extract of U. prolifera (30% PeUP). Rat primary chondrocytes were pre-treated with 30% PeUP for 1 h before interleukin-1ß (10 ng/mL) stimulation. The production of nitrite, prostaglandin E2 (PGE2), collagen type II (Col II), and aggrecan (ACAN) were detected by Griess reagent and enzyme-linked immunosorbent assay. The protein expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-1, MMP-3, MMP-13, a disintegrin and metalloproteinase with thrombospondin (ADAMTS)-4, ADAMTS-5, and mitogen-activated protein kinases (MAPKs) (extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, and p38) were assessed by western blot. Thirty percent of PeUP significantly inhibited the expression of nitrite, iNOS, PGE2, COX-2, MMP-1, MMP-3, MMP-13, ADMATS-4, and ADMATS-5 in interleukin (IL)-1ß-stimulated chondrocytes. Moreover, 30% PeUP decreased the IL-1ß-induced degradation of Col II and ACAN. Additionally, 30% of PeUP suppressed IL-1ß-induced phosphorylation of MAPKs. Therefore, 30% PeUP is a potential therapeutic agent to mitigate OA progression.

Few-shot learning: temporal scaling in behavioral and dopaminergic learning.

How do we learn associations in the world (e.g., between cues and rewards)? Cue-reward associative learning is controlled in the brain by mesolimbic dopamine1-4. It is widely believed that dopamine drives such learning by conveying a reward prediction error (RPE) in accordance with temporal difference reinforcement learning (TDRL) algorithms5. TDRL implementations are "trial-based": learning progresses sequentially across individual cue-outcome experiences. Accordingly, a foundational assumption-often considered a mere truism-is that the more cue-reward pairings one experiences, the more one learns this association. Here, we disprove this assumption, thereby falsifying a foundational principle of trial-based learning algorithms. Specifically, when a group of head-fixed mice received ten times fewer experiences over the same total time as another, a single experience produced as much learning as ten experiences in the other group. This quantitative scaling also holds for mesolimbic dopaminergic learning, with the increase in learning rate being so high that the group with fewer experiences exhibits dopaminergic learning in as few as four cue-reward experiences and behavioral learning in nine. An algorithm implementing reward-triggered retrospective learning explains these findings. The temporal scaling and few-shot learning observed here fundamentally changes our understanding of the neural algorithms of associative learning.

The Effectiveness of Virtual Reality Intervention for COVID-19-Related Psychological Distress: A Systematic Review.

OBJECTIVE: The prolonged coronavirus disease-2019 (COVID-19) pandemic is likely to cause psychological distress in people. This systematic review aimed to identify the effectiveness of virtual reality (VR)-based psychological intervention among individuals with psychological distress during the COVID-19 crisis. PubMed, Ovid MEDLINE, Cochrane Library, Web of Science, Embase, and PsycINFO databases were searched for articles published until July 2022. METHODS: The available citations were deduplicated and screened by two authors using the title and abstract information. Eligibility criteria were constructed according to the PICOT guidelines. Empirical studies of all designs and comparator groups were included if they appraised the impact of an immersive VR intervention on any standardized measure indicative of psychological distress (stress, anxiety, depression, and post-traumatic symptoms) or improvements in quality of life in participants, including COVID-19 patients, medical staff working with COVID-19 patients, and people who had experienced strict social distancing during the COVID-19 pandemic. RESULTS: The results were discussed using a narrative synthesis because of the heterogeneity between studies. Seven of the studies met the inclusion criteria. There were two randomized controlled trials and five uncontrolled studies on VR interventions. CONCLUSION: All studies reported significant improvement in a wide range of psychological distress during COVID-19, ranging from stress, anxiety, depression, and post-traumatic symptoms to quality of life, supporting the efficacy of VR-based psychological intervention. Our results suggest that VR intervention has potential to ameliorate COVID-19-related psychological distress with efficacy and safety.

Smart soft contact lenses for continuous 24-hour monitoring of intraocular pressure in glaucoma care.

Continuous monitoring of intraocular pressure, particularly during sleep, remains a grand challenge in glaucoma care. Here we introduce a class of smart soft contact lenses, enabling the continuous 24-hour monitoring of intraocular pressure, even during sleep. Uniquely, the smart soft contact lenses are built upon various commercial brands of soft contact lenses without altering their intrinsic properties such as lens power, biocompatibility, softness, transparency, wettability, oxygen transmissibility, and overnight wearability. We show that the smart soft contact lenses can seamlessly fit across different corneal curvatures and thicknesses in human eyes and therefore accurately measure absolute intraocular pressure under ambulatory conditions. We perform a comprehensive set of in vivo evaluations in rabbit, dog, and human eyes from normal to hypertension to confirm the superior measurement accuracy, within-subject repeatability, and user comfort of the smart soft contact lenses beyond current wearable ocular tonometers. We envision that the smart soft contact lenses will be effective in glaucoma care.

Correlation between Stress and Anxiety to Viral Epidemics (SAVE) and Burnout among Korean Dental Hygienists during the COVID-19 Pandemic: A Cross-Sectional Study.

This study aimed to investigate the correlations among Stress and Anxiety to Viral Epidemics (SAVE), job stress (JS), and burnout among Korean dental hygienists during the COVID-19 pandemic and to identify the moderating effect of JS. As a cross-sectional study, a self-reporting questionnaire was used to survey 204 clinical dental hygienists to measure the levels of SAVE, JS, and burnout, along with their demographic characteristics as the control variables. Pearson correlation analysis and hierarchical multiple regression analysis were performed to analyse the correlations among burnout, SAVE, and JS, including the moderating effect of JS. With education level and subjective health controlled, JS (ß = 1.05, p < 0.001), SAVE (ß = 0.69, p = 0.020) and the interaction between SAVE and JS (ß = −0.93, p = 0.050) were identified as significant influencing factors of burnout. The adjusted explanatory power of the model was found to be 52.4%. In summary, both SAVE and JS were significant influencing factors of burnout among dental hygienists, while a moderating effect of JS was also identified. Therefore, it is necessary to create a work environment that can relieve SAVE and JS to reduce burnout among dental hygienists.

Chondroprotective Effects of 4,5-Dicaffeoylquinic Acid in Osteoarthritis through NF-κB Signaling Inhibition.

Osteoarthritis (OA) is characterized by cartilage degradation, inflammation, and pain. The dicaffeoylquinic acid (diCQA) isomer, 4,5-diCQA, exhibits antioxidant activity and various other health-promoting benefits, but its chondroprotective effects have yet to be elucidated. In this study, we aimed to investigate the chondroprotective effects of 4,5-diCQA on OA both in vitro and in vivo. Primary rat chondrocytes were pre-treated with 4,5-diCQA for 1 h before stimulation with interleukin (IL)-1ß (5 ng/mL). The accumulation of nitrite, PGE2, and aggrecan was observed using the Griess reagent and ELISA. The protein levels of iNOS, COX-2, MMP-3, MMP-13, ADMATS-4, MAPKs, and the NF-κB p65 subunit were measured by Western blotting. In vivo, the effects of 4,5-diCQA were evaluated for 2 weeks in a destabilization of the medial meniscus (DMM)-surgery-induced OA rat model. 4,5-diCQA significantly inhibited IL-1ß-induced expression of nitrite, iNOS, PGE2, COX-2, MMP-3, MMP-13, and ADAMTS-4. 4,5-diCQA also decreased the IL-1ß-induced degradation of aggrecan. It also suppressed the IL-1ß-induced phosphorylation of MAPKs and translocation of the NF-κB p65 subunit to the nucleus. These findings indicate that 4,5-diCQA inhibits DMM-surgery-induced cartilage destruction and proteoglycan loss in vivo. 4,5-diCQA may be a potential therapeutic agent for the alleviation of OA progression. In this study, diclofenac was set to be administered once every two days, but it showed an effect on OA. These results may be used as basic data to suggest a new dosing method for diclofenac.

Effect of Proton Pump Inhibitor on the Outcome of Laryngeal Microsurgery in Patients With Vocal Fold Mucosal Disease With Reflux Symptoms.

OBJECTIVES: To evaluate the effect of proton pump inhibitor (PPI) after laryngeal microsurgery (LMS) in patients with benign vocal fold (VF) mucosal disease and in patients with overt reflux symptom according to subjective and objective voice assessment. METHODS: The improvement of voice handicap index-10 (VHI-10) score, reflux symptom index (RSI) score, grade, roughness, breathiness, asthenia, and strain (GRBAS) score, Jitter, Shimmer, noise to harmonics ratio (NHR), maximum phonation time of acoustic voice analysis RESULTS: A total of 47 patients (PPI group [n = 24] and non-PPI group [n = 23]) completed the study. The scores for VHI-10, RSI, GRBAS, and acoustic parameters significantly improved in both groups after surgery. In the subgroup analysis of patients with overt reflux symptoms (RSI ≥ 13; non-PPI group [n = 12], PPI group [n = 15]), significant between-group differences were observed in terms of the improvement in NHR and the strain factor. CONCLUSION: Postoperative PPI administration in patients with VF benign mucosal disease with reflux symptoms might improve subjective and objective voice outcomes after LMS.

Cynaroside protects human periodontal ligament cells from lipopolysaccharide-induced damage and inflammation through suppression of NF-κB activation.

OBJECTIVE: To investigate whether cynaroside protects human periodontal ligament (hPDL) cells from lipopolysaccharide (LPS)-induced damage and inflammation and to analyze the underlying mechanism. METHODS: LPS was used to stimulate hPDL and RAW264.7 cells. MTT assay was used to detect cell viability, and protein expression levels were measured via western blot analysis. Nitrite oxide and prostaglandin E2 were used to quantify the inflammatory response. Alizarin Red S staining was used to detect mineralized nodules. RESULTS: Cynaroside inhibited the expression of iNOS, COX-2, TNF-α, and IL-6 in LPS-stimulated hPDL and RAW264.7 cells without cytotoxicity. Furthermore, cynaroside significantly suppressed LPS-induced protein expression of matrix metalloproteinase 3. Additionally, cynaroside prevented LPS-induced NF-κB p65 subunit translocation to the nucleus by inhibiting the phosphorylation and degradation of IκB-α. Moreover, cynaroside could restore the mineralization ability of hPDL cells reduced by LPS. CONCLUSION: Cynaroside protected hPDL cells from LPS-induced damage and inflammation via inhibition of NF-κB activation. These results suggest that cynaroside may be a potential therapeutic agent for the alleviation of periodontitis.

Chondroprotective Effect of Cynaroside in IL-1ß-Induced Primary Rat Chondrocytes and Organ Explants via NF-κB and MAPK Signaling Inhibition.

Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage degradation and inflammation. Interleukin-1ß is the key player in the pathogenesis of OA, which induces the expression of various catabolic factors that contribute to cartilage degradation. Cynaroside (luteolin-7-O-glucoside or luteoloside) is a flavonoid that has various pharmacological properties, such as antitumor, anti-inflammatory, and antioxidant activities. In this study, we investigated the chondroprotective effects of cynaroside on IL-1ß-stimulated chondrocytes and organ explants. The production of nitrite, PGE2, collagen type II, and aggrecan was measured by a Griess reagent and ELISAs, and the production of ROS was measured by H2DCF-DA fluorescence. The protein levels of iNOS, Cox-2, MMP-1, MMP-3, MMP-13, ADAMTS-4, MAPKs, and the NF-κB p65 subunit were measured by western blot. Proteoglycan analysis was performed by Alcian Blue staining (in vitro) and Safranin O staining (ex vivo). Cynaroside inhibited IL-1ß-induced expression of catabolic factors (nitrite, iNOS, ROS, PGE2, Cox-2, MMP-1, MMP-3, MMP-13, and ADAMTS-4) and degradation of anabolic factors (collagen type II and aggrecan). Furthermore, cynaroside suppressed IL-1ß-induced phosphorylation of MAPKs and translocation of the NF-κB p65 subunit into the nucleus. Collectively, these results suggest that cynaroside may be a potential candidate for the development of new therapeutic drugs for the alleviation of OA progression.

Anti-inflammatory potential of Trifolium pratense L. leaf extract in LPS-stimulated RAW264.7 cells and in a rat model of carrageenan-induced inflammation.

This study evaluated the anti-inflammatory potential of a 40% prethanol extract of Trifolium pratense leaves (40% PeTP) using in vitro (RAW264.7 cells) and in vivo (carrageenan-induced inflammation model) experiments. Pretreatment with 40% PeTP significantly inhibited the LPS-induced expression of nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and inflammatory cytokines, including tumour necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 in RAW264.7 cells, without inducing cytotoxicity. The inhibitory effects of 40% PeTP are mediated through suppression of the nuclear translocation of nuclear factor (NF)-κB and the phosphorylation of mitogen-activated protein kinases (MAPKs). Oral administration of 40% PeTP at 50, 100, and 200 mg/kg of body weight suppressed carrageenan-induced oedema in a dose-dependent manner. Collectively, our results suggested that 40% PeTP exerts potential anti-inflammatory effects by suppressing the activation of the NF-κB and MAPK pathways in vitro, and by reducing carrageenan-induced paw oedema in vivo.

Reversine induces caspase-dependent apoptosis of human osteosarcoma cells through extrinsic and intrinsic apoptotic signaling pathways.

BACKGROUND: The 2-(4-morpholinoanilino)-6-cyclohexylaminopurine (reversine) acts as a chemopreventive agent and induces apoptotic cell death in various cancer cells. However, the anticancer effects of reversine on osteosarcoma cells are not clearly established. OBJECTIVE: The purpose of this study was to investigate the effect of reversine on cell proliferation and induction of apoptosis in human osteosarcoma cells. METHODS: Cell viability assay, histological analysis, DAPI staining, caspase activation analysis, flow cytometric analysis and immunoblotting were carried out in MG-63 osteosarcoma cells. RESULTS: Reversine inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Reversine-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was significantly up-regulated by reversine treatment. Moreover, the caspase-8, a part of the extrinsic apoptotic pathway, was activated by reversine treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria dependent intrinsic apoptosis pathway, significantly decreased following reversine treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9 increased by reversine treatments. In addition, reversine activated caspase-3 and Poly (ADP-ribose) polymerase (PARP) to induce cell death. The Z-VAD-fmk significantly inhibited cell death through the suppression of caspase-3 expression in MG-63 cells treated with reversine. CONCLUSION: These results suggest that the reversine may inhibit cell proliferation and induce apoptotic cell death in MG-63 osteosarcoma cells through both the mitochondria-mediated intrinsic pathway and the death receptor-mediated extrinsic pathway, and may have potential properties for the discovery of anti-cancer agents.

Erratum: Adenosine induces intrinsic apoptosis via the PI3K/Akt/mTOR signaling pathway in human pharyngeal squamous carcinoma FaDu cells.

[This corrects the article DOI: 10.3892/ol.2018.8089.].

MicroRNA-203 Induces Apoptosis by Targeting Bmi-1 in YD-38 Oral Cancer Cells.

BACKGROUND/AIM: MicroRNAs (miRNAs) are closely associated with a number of cellular processes, including cell development, differentiation, proliferation, carcinogenesis, and apoptosis. The aim of the present study was to elucidate the molecular mechanisms underlying the tumor suppressor activity of miRNA-203 (miR-203) in YD-38 human oral cancer cells. MATERIALS AND METHODS: Polymerase chain reaction analysis, MTT assay, DNA fragmentation assay, fluorescence-activated cell-sorting analysis, gene array, immunoblotting, and luciferase assay were carried out in YD-38 cells. RESULTS: miR-203 expression was significantly down-regulated in YD-38 cells compared to expression levels in normal human oral keratinocytes. miR-203 decreased the viability of YD-38 cells in a time- and dose-dependent manner. In addition, over-expression of miR-203 significantly increased not only DNA segmentation, but also the apoptotic population of YD-38 cells. These results indicate that miR-203 overexpression induces apoptosis in YD-38 cells. Target gene array analysis revealed that the expression of the polycomb complex protein gene Bmi-1, a representative oncogene, was significantly down-regulated by miR-203 in YD-38 cells. Moreover, both mRNA and protein levels of Bmi-1 were significantly reduced in YD-38 cells transfected with miR-203. These results indicate that Bmi-1 is a target gene of miR-203. A luciferase reporter assay confirmed that miR-203 suppressed Bmi-1 expression by directly targeting the 3'-untranslated region. CONCLUSION: miR-203 induces apoptosis in YD-38 cells by directly targeting Bmi-1, which suggests its possible application as an anti-cancer therapeutic.

Chondroprotective effects of aqueous extract of Anthriscus sylvestris leaves on osteoarthritis in vitro and in vivo through MAPKs and NF-κB signaling inhibition.

Osteoarthritis (OA) is a common degenerative joint disease, characterized by cartilage degradation and inflammation, in the elderly population. Anthriscus sylvestris has been used in Korean traditional medicine and contains many polyphenolic compounds such as cynaroside and chlorogenic acid, which are major active components responsible for its antioxidant effect. In this study, we aimed to evaluate the chondroprotective effect of an aqueous extract of A. sylvestris leaves (AE-ASL) on OA, both in vitro and in vivo. Rat primary chondrocytes were pretreated with AE-ASL for 1 h before interleukin-1ß (20 ng/mL) stimulation. The production of nitrite, PGE2, aggrecan, and collagen type II were detected by Griess reagent and ELISAs. The mRNA levels of iNOS, COX-2, MMP-3, and MMP-13 were measured by RT-PCR. In addition, protein levels of iNOS, COX-2, MMP-3, MMP-13, ADAMTS-4, MAPKs, and NF-κB p65 subunit were measured by western blot analysis. Sulfated glycosaminoglycan (sGAGs) were detected by dimethylmethylene blue (DMMB) assay. During in vivo study, the effects of AE-ASL were evaluated for 8 weeks in a rat model of destabilization of the medial meniscus (DMM) surgery-induced OA. AE-ASL significantly inhibited expression of nitrite, iNOS, PGE2, COX-2, MMP-3, MMP-13, and ADAMTS-4 in IL-1ß-stimulated chondrocytes. Moreover, it decreased the IL-1ß-induced degradation of aggrecan, collagen type II, and proteoglycan. In addition, AE-ASL suppressed IL-1ß-induced phosphorylation of MAPKs and NF-κB p65 subunit translocation to nucleus. In vivo, AE-ASL inhibited DMM surgery-induced cartilage destruction and proteoglycan loss. Taken together, these results suggest that AE-ASL may be a potential therapeutic agent for the alleviation of OA progression.

Adenosine induces intrinsic apoptosis via the PI3K/Akt/mTOR signaling pathway in human pharyngeal squamous carcinoma FaDu cells.

Adenosine has been identified to occur abundantly intra-and extracellularly, and to exert diverse biological functions, including the suppression of cell proliferation and the induction of apoptosis. Adenosine has been reported to induce apoptosis in several cancer cell lines; however, to the best of our knowledge, the effect of adenosine on head and neck cancer cells has not been investigated. Therefore, the purpose of the present study was to evaluate whether adenosine exerts any anticancer effect via induction of apoptosis in human pharyngeal squamous carcinoma FaDu cells. An MTT assay demonstrated that adenosine-treated FaDu cells inhibited a dose-dependent rate of cell growth, whereas human oral keratinocytes cells were unaffected by adenosine treatment. In addition, A1 and A2a adenosine receptor mRNA was detected in FaDu cells by reverse transcription-polymerase chain reaction, and adenosine-induced FaDu cell death was significantly suppressed by treatment with ATL-444, an antagonist of these receptors. Furthermore, adenosine-induced cell growth inhibition was exerted via apoptosis, as confirmed by the analysis of DNA fragmentation, Hoechst nuclear staining and flow cytometry with Annexin V-fluorescein isothiocyanate and propidium iodide staining. Adenosine was also demonstrated to induce an increase in Bcl-associated X expression, a decrease in B-cell lymphoma 2 expression, the release of cytochrome c from mitochondria, and the activation of caspase-3, -9 and poly(ADP-ribose) polymerase in FaDu cells. Finally, phosphoinositide 3-kinase (PI3K), RAC serine/threonine-protein kinase (Akt) and mechanistic target of rapamycin (mTOR) phosphorylation was found to be significantly inhibited in adenosine-treated FaDu cells, as was phosphorylation of the mTOR downregulators, S6 kinase ß1, eukaryotic translation initiation factor 4E-binding protein 1, and eukaryotic translation initiation factor 4 γ1. Taken together, these results indicate that adenosine induces apoptosis via the mitochondrial intrinsic pathway, and activates caspase-3 and -9 activity via the PI3K/Akt/mTOR signaling pathway.

Anthricin­induced caspase­dependent apoptosis through IGF1R/PI3K/AKT pathway inhibition in A549 human non­small lung cancer cells.

Anthricin (deoxypodophyllotoxin) is a major lignan in Anthriscus sylvestris and possesses many bioactivities such as antiproliferative, antitumor, anti­platelet aggregation, antiviral and anti­inflammatory actions. However, the anticancer effects of anthricin on A549 human non­small cell lung cancer cells and potential molecular mechanisms remain unknown. Therefore, we investigated the anticancer effect of anthricin and the underlying mechanism in A549 cells. Anthricin (10­200 nM) inhibited the viability of A549 cells in a dose­ and time­dependent manner. Moreover, anthricin­induced apoptosis was confirmed by live and dead assay, 4,6­dianmidino­2­phenylindole staining, and flow cytometric analysis. In addition, anthricin induced cell cycle arrest at the G2/M phase through suppression of the expression of cell cycle cascade proteins, Cdc2 and Cdc25C. Furthermore, it induced the expression of caspase­related proteins and significantly suppressed the phosphorylation of insulin­like growth factor 1 receptor (IGF1R), PI3K and Akt. Anthricin significantly inhibited tumor growth without any significant change in the body weight of mice in A549 tumor xenograft BALB/c nude mice. Anthricin induced caspase­dependent apoptosis through the IGF1R/PI3K/Akt signaling pathway in A549 cells.

Oleamide suppresses inflammatory responses in LPS-induced RAW264.7 murine macrophages and alleviates paw edema in a carrageenan-induced inflammatory rat model.

Oleamide compounds purified from green algae have been used for the prevention and treatment of atherosclerosis, thrombosis, arthritis, and cancer. They function through their metabolic conversion into prostaglandins, thromboxanes, and leukotrienes. However, the actual mechanism of action has not been well characterized. To investigate the underlying anti-inflammatory activity and associated mechanisms, oleamide purified from Codium fragile was studied using RAW264.7 murine macrophages and a carrageenan-induced inflammatory rat model. Our results indicate that pre-treatment of RAW264.7 cells with oleamide significantly suppressed LPS-induced nitrite production and PGE2 secretion. Oleamide inhibited LPS-induced iNOS and COX-2 mRNA and protein expression. It also inhibited the LPS-induced production of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, and IL-6. In addition, oleamide prevented the nuclear translocation of NF-κB by suppressing the phosphorylation of the inhibitor of kappa B (IκB)-α. Oleamide also suppressed the phosphorylation of mitogen-activated protein kinases such as ERK1/2 and JNK. Furthermore, inhibition of paw swelling (%) was suppressed 2 h after the intraperitoneal injection of oleamide (20 mg/kg, body weight) in a carrageen-induced rat model. Therefore, our results suggest that oleamide can be used as a single ingredient treatment for inflammatory diseases.