• Title/Summary/Keyword: COX-2 activity

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Anti-Inflammatory Activity of Ethanol Extract of Sargassum miyabei Yendo via Inhibition of NF-κB and MAPK Activation (NF-κB와 MAPKs 활성 저해를 통한 미야베 모자반(Sargassum miyabei Yendo) 에탄올 추출물의 항염증 활성)

  • Kim, Min-Ji;Bae, Nan-Young;Kim, Koth-Bong-Woo-Ri;Park, Sun-Hee;Jang, Mi-Ran;Im, Moo-Hyeog;Ahn, Dong-Hyun
    • Microbiology and Biotechnology Letters
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    • v.44 no.4
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    • pp.442-451
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    • 2016
  • The aim of this study was to investigate the anti-inflammatory effect of Sargassum miyabei Yendo ethanol extract (SMYEE) using RAW 264.7 cells and croton oil-induced Balb/c mice. SMYEE inhibited the production of pro-inflammatory cytokines [interleukin (IL)-6, tumor necrosis factor $(TNF)-{\alpha}$, and $IL-1{\beta}$] and nitric oxide in lipopolysaccharide (LPS)-induced inflammatory response. In addition, SMYEE suppressed the expression of inducible nitric oxide, cyclooxygenase-2, and nuclear factor-kappa B. Further, SMYEE inhibited the expression of mitogen-activated protein kinases (MAPKs), such as extra cellular signal-regulated kinase 1/2, p38, and c-Jun N-terminal kinase. In ear edema test, edema formation in the SMYEE treatment was lower than that in the positive control and was similar to that in the prednisolone treatment group. Photomicrographs of mice ear tissue showed a reduction in dermal thickness and number of infiltrated mast cells. Therefore, our results indicate that SMYEE exerts an anti-inflammatory effect via inhibition of nuclear factor ${NF}-{\kappa}B$ and MAPK activation and can be used as a natural source of anti-inflammatory compounds.

Ammonia Decomposition over Ni Catalysts Supported on Zeolites for Clean Hydrogen Production (청정수소 생산을 위한 암모니아 분해 반응에서 Ni/Zeolite 촉매의 반응활성에 관한 연구)

  • Jiyu Kim;Kyoung Deok Kim;Unho Jung;Yongha Park;Ki Bong Lee;Kee Young Koo
    • Journal of the Korean Institute of Gas
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    • v.27 no.3
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    • pp.19-26
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    • 2023
  • Hydrogen, a clean energy source free of COx emissions, is poised to replace fossil fuels, with its usage on the rise. Despite its high energy content per unit mass, hydrogen faces limitations in storage and transportation due to its low storage density and challenges in long-term storage. In contrast, ammonia offers a high storage capacity per unit volume and is relatively easy to liquefy, making it an attractive option for storing and transporting large volumes of hydrogen. While NH3 decomposition is an endothermic reaction, achieving excellent low-temperature catalytic activity is essential for process efficiency and cost-effectiveness. The study examined the effects of different zeolite types (5A, NaY, ZSM5) on NH3 decomposition activity, considering differences in pore structure, cations, and Si/Al-ratio. Notably, the 5A zeolite facilitated the high dispersion of Ni across the surface, inside pores, and within the structure. Its low Si/Al ratio contributed to abundant acidity, enhancing ammonia adsorption. Additionally, the presence of Na and Ca cations in the support created medium basic sites that improved N2 desorption rates. As a result, among the prepared catalysts, the 15 wt%Ni/5A catalyst exhibited the highest NH3 conversion and a high H2 formation rate of 23.5 mmol/gcat·min (30,000 mL/gcat·h, 600 ℃). This performance was attributed to the strong metal-support interaction and the enhancement of N2 desorption rates through the presence of medium basic sites.

Co-immunomodulatory Activities of Anionic Macromolecules Extracted from Codium fragile with Red Ginseng Extract on Peritoneal Macrophage of Immune-Suppressed Mice

  • Kim, Ji Eun;Monmai, Chaiwat;Rod-in, Weerawan;Jang, A-yeong;You, Sang-Guan;Lee, Sang-min;Jung, Seok-Kyu;Park, Woo Jung
    • Journal of Microbiology and Biotechnology
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    • v.30 no.3
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    • pp.352-358
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    • 2020
  • In this study we investigated the immune effects of oral administration of anionic macromolecules extracted from Codium fragile (CFAM) and red ginseng extract mixture on the peritoneal macrophage cells in immune-suppressed mice. Cyclophosphamide (CY) induces the immune-suppressed condition. CY-treated mice were orally fed with different concentrations of CFAM supplemented with red ginseng extract and the peritoneal macrophages collected. CY treatment significantly decreased the immune activities of peritoneal macrophages, compared to the normal mice. The administration of CFAM mixed with red ginseng extract significantly boosted the viability of macrophage cells and nitric oxide production of peritoneal macrophages. Further, the oral administration of CFAM mixed with red ginseng extract up-regulated the expression of iNOS, COX-2, and TLR-4 as well as cytokines such as IL-1β, IL-6, TNF-α, and IFN-γ more than the red ginseng-treated group. This study showed that CFAM enhanced the immune activity of red ginseng extract in the peritoneal macrophage cells of immune-suppressed mice. Furthermore, CFAM might be used as a co-stimulant of red ginseng extract through the regulation of macrophage cells for the enhancement of human health and immunity.

The Experimental Study on Anti-oxidant and Anti-inflammatory Effect Hyulbuchukeotanggamibang (HBCT) (혈부축어탕가미방(血府逐瘀湯加味方)의 염증(炎症) 병리(病理) 인자(因子)와 산화력(酸化力) 손상(損傷)에 미치는 영향)

  • Han, Hye-Suk;Lim, Hyun-Jung;Shin, Sun-Mi;Kim, Soo-Min;Lee, Jung-Eun;Yoo, Dong-Youl
    • The Journal of Korean Obstetrics and Gynecology
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    • v.21 no.1
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    • pp.99-116
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    • 2008
  • Purpose: This study was performed to evaluate anti-inflammatory effects of Hyulbuchukeotanggamibang water extract (HBCT). Methods: In the study of anti-inflammatory effects, HBCT was investigated using cultured cells and a 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 determined in mouse lung fibroblast cells (mLFCs) and RAW264.7 cells. Results: Prior to the experiment, we investigated the cytotoxicity of HBCT. HBCT showed a safety in cytotoxicity on mLFCs. In experiment of anti-inflammatory effect, HBCT effected scavenging activity on DPPH free radical, superoxide dismutase and superoxide anion radical. HBCT inhibited $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, COX-2 and NOS-II mRNA expression in a concentration-dependent manner in RAW264.7 cell line, and inhibited significantly $IL-1{\beta}$, IL-6, $TNF-{\alpha}$ production at $100{\mu}g/\;ml$ in a concentration-dependent manner. Conclusion: These results suggest that HBCT can be used for treating diverse female diseases caused by inflammation such as endometriosis, pelvic pain, cervicitis, pelvic inflammatory disease and pelvic tuberculosis and so forth.

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Simvastatin Reduces Lipopolysaccharides-Accelerated Cerebral Ischemic Injury via Inhibition of Nuclear Factor-kappa B Activity

  • Jalin, Angela M.A. Anthony;Lee, Jae-Chul;Cho, Geum-Sil;Kim, Chunsook;Ju, Chung;Pahk, Kisoo;Song, Hwa Young;Kim, Won-Ki
    • 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.

Risk of Cancer Mortality according to the Metabolic Health Status and Degree of Obesity

  • Oh, Chang-Mo;Jun, Jae Kwan;Suh, Mina
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.22
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    • pp.10027-10031
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    • 2014
  • Background: We investigated the risk of cancer mortality according to obesity status and metabolic health status using sampled cohort data from the National Health Insurance system. Materials and Methods: Data on body mass index and fasting blood glucose in the sampled cohort database (n=363,881) were used to estimate risk of cancer mortality. Data were analyzed using a Cox proportional hazard model (Model 1 was adjusted for age, sex, systolic blood pressure, diastolic blood pressure, total cholesterol level and urinary protein; Model 2 was adjusted for Model 1 plus smoking status, alcohol intake and physical activity). Results: According to the obesity status, the mean hazard ratios were 0.82 [95% confidence interval (CI), 0.75-0.89] and 0.79 (95% CI, 0.72-0.85) for the overweight and obese groups, respectively, compared with the normal weight group. According to the metabolic health status, the mean hazard ratio was 1.26 (95% CI, 1.14-1.40) for the metabolically unhealthy group compared with the metabolically healthy group. The interaction between obesity status and metabolic health status on the risk of cancer mortality was not statistically significant (p=0.31). Conclusions: We found that the risk of cancer mortality decreased according to the obesity status and increased according to the metabolic health status. Given the rise in the rate of metabolic dysfunction, the mortality from cancer is also likely to rise. Treatment strategies targeting metabolic dysfunction may lead to reductions in the risk of death from cancer.

Anti-oxidative properties of ginseng (인삼의 항산화 작용)

  • Kim, Eun-Hye;Rhee, Dong-Kwon
    • Journal of Ginseng Research
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    • v.33 no.1
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    • pp.1-7
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    • 2009
  • Clinical and animal studies have shown that free radical overload is an important cause for a variety of diseases. Although ginseng has been recognized as antioxidant, how it modulates anti-oxidative process at the molecular level remains unknown. Free radical production is induced by tumor necrosis factor-$\alpha$ (TNF-$\alpha$) under the stress condition, and (TNF-$\alpha$) release is activated by TNF-$\alpha$-converting enzyme (TACE). Since TACE inhibitor is also well known for anti-inflammatory agent, ginseng seems to show anti-oxidative activity by repressing TACE pathway. Further studies on signal transduction would be warranted to elucidate molecular action mechanisms of ginseng on anti-oxidation and anti-inflammation.

The Effects of Gokgisaeng on Anti-inflammation and Rat C6 Glioma Cell Migration (곡기생(槲寄生)의 항염증 효능 및 암세포 이주저해에 미치는 영향)

  • Kim, Hyun-Young;Jang, Soo-Young;Jeong, Ji-Cheon;Shin, Hyeon-Cheol
    • The Journal of Internal Korean Medicine
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    • v.34 no.1
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    • pp.31-45
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    • 2013
  • Objectives : Gokgisaeng (Korean mistletoe) is used for the treatment of inflammatory and cancer diseases in traditional Korean medicine and its major component lectins have been reported to induce nitric oxide (NO) in RAW 264.7 macrophages, and also induce apoptosis of various types of cancer cells, although its modulatory effects on cancer cell migration and macrophage activation is poorly understood. The aim of this study is to clarify molecular mechanisms of action responsible for the anti-inflammatory and antitumor migration potentials of Korean mistletoe extract (KME). Methods : We investigated the anti-inflammatory activity of KME on NO production and inducible nitric oxide synthase (iNOS) expression by lipopolysaccharide (LPS) in both RAW 264.7 macrophages and rat C6 glioma cells, and also evaluated inhibitory efficacy on glioma cell growth and migration. For assessment, XTT assay, nitrite assay, RT-PCR, scratch-wound and Boyden chamber assay, and western blot analysis were performed. Results : Previously reported, unlike the efficacy of Gokgisaeng lectin, KME inhibited NO production and iNOS expression, and suppressed pro-inflammatory mediators including IL-$1{\beta}$, IL-6, COX-2, iNOS in LPS-stimulated RAW 264.7 cells. Furthermore, KME suppressed tumor cell growth and migration, and it also inhibited LPS-induced NO release and iNOS activation by down-regulating expression of protein kinase C (PKC) and phosphorylation of ERK in C6 glioma cells. Conclusions : Our research findings provide evidence that KME can play a significant role in blocking pro-inflammatory reaction and malignant progression of tumors through the suppression of NO/iNOS by down-regulating of inflammatory signaling pathways, PKC/ERK.

Obesity and Obese-related Chronic Low-grade Inflammation in Promotion of Colorectal Cancer Development

  • Pietrzyk, Lukasz;Torres, Anna;Maciejewski, Ryszard;Torres, Kamil
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.10
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    • pp.4161-4168
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    • 2015
  • Colorectal cancer (CRC) is a worldwide health problem, being the third most commonly detected cancer in males and the second in females. Rising CRC incidence trends are mainly regarded as a part of the rapid 'Westernization' of life-style and are associated with calorically excessive high-fat/low-fibre diet, consumption of refined products, lack of physical activity, and obesity. Most recent epidemiological and clinical investigations have consistently evidenced a significant relationship between obesity-driven inflammation in particular steps of colorectal cancer development, including initiation, promotion, progression, and metastasis. Inflammation in obesity occurs by several mechanisms. Roles of imbalanced metabolism (MetS), distinct immune cells, cytokines, and other immune mediators have been suggested in the inflammatory processes. Critical mechanisms are accounted to proinflammatory cytokines (e.g. IL-1, IL-6, IL-8) and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$). These molecules are secreted by macrophages and are considered as major agents in the transition between acute and chronic inflammation and inflammation-related CRC. The second factor promoting the CRC development in obese individuals is altered adipokine concentrations (leptin and adiponectin). The role of leptin and adiponectin in cancer cell proliferation, invasion, and metastasis is attributable to the activation of several signal transduction pathways (JAK/STAT, mitogen-activated protein kinase (MAPK), phosphatidylinositol 3 kinase (PI3K), mTOR, and 5'AMPK signaling pathways) and multiple dysregulation (COX-2 downregulation, mRNA expression).

Anti-Inflammatory Effect of Alginate Oligosaccharides Produced by an Alginate-Degrading Enzyme from Shewanella oneidensis PKA1008 on LPS-Induced RAW 264.7 Cells (Shewanella oneidensis PKA1008 유래 알긴산 분해 효소에 의해 제조된 알긴산 올리고당의 항염증 효과)

  • Kim, Min-Ji;Bae, Nan-Yong;Bark, Si-Woo;Kim, Koth-Bong-Woo-Ri;Park, Ji-Hye;Park, Sun-Hee;Ahn, Dong-Hyun
    • Korean Journal of Fisheries and Aquatic Sciences
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    • v.48 no.6
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    • pp.888-897
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    • 2015
  • The anti-inflammatory effect of alginate oligosaccharides on LPS-induced RAW 264.7 cells was investigated at different time points (0-60 h). The alginate oligosaccharides were produced by an alginate-degrading enzyme from Shewanella oneidensis PKA1008. The alginate oligosaccharides decreased the production of nitric oxide and proinflammatory cytokines [tumor necrosis factor-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-6] in a dose-dependent manner. The alginate oligosaccharides showed peak anti-inflammatory activity after 36 h of incubation; at that time point, reduced protein expression of NF-${\kappa}B$ p65, iNOS, and COX-2 was detected. Furthermore, the alginate oligosaccharide treatment reduced the formation of ear edema at 36 h compared to samples examined at 0 h when the oligosaccharides were administered at 50 and 250 mg/kg body weight, as well as dermal thickness and mast cell numbers in a histological analysis. These results suggest that alginate oligosaccharides are a promising anti-inflammatory agent.