• Title/Summary/Keyword: COX-1, COX-2

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Effect of Sulfur Enriched Young Radish Kimchi on the Induction of Apoptosis in AGS Human Gastric Adenocarcinoma Cells

  • Bak, Soon-Sun;Kong, Chang-Suk;Rhee, Sook-Hee;Rho, Chi-Woong;Kim, Nak-Ku;Choi, Keyng-Lag;Park, Kun-Young
    • Preventive Nutrition and Food Science
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    • v.12 no.2
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    • pp.79-83
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    • 2007
  • The effects of young radish (YR, yeolmu in Korean) on the induction of apoptosis were examined in AGS human gastric adenocarcinoma cells. The young radish kimchi (YRK) were made of YR cultivated in the soil without (Control YR kimchi: C-YRK) and with 1,818 g/m$^{3}$ sulfur (Sulfur YR kimchi: S-YRK), respectively. Methanol extracts from S-YRK exhibited higher inhibitory effect on the growth of AGS human gastric adenocarcinoma cells in a time dependent-manner compared to C-YRK at the same concentration. 4,6-diamidino-2-phenylindole (DAPI) staining showed that S-YRK induced apoptosis accompanied by the increased Bax but decreased Bcl-2 in mRNA expression. Moreover, S-YRK decreased the levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNA expressions. The results suggested that S-YRK cultivated in the presence of sulfur elicited stronger anticancer activity than C-YRK in vitro. Dietary intakes of S-YRK may be beneficial to decrease the risk of cancer.

Ginsenoside Rg3 ameliorates allergic airway inflammation and oxidative stress in mice

  • Huang, Wen-Chung;Huang, Tse-Hung;Yeh, Kuo-Wei;Chen, Ya-Ling;Shen, Szu-Chuan;Liou, Chian-Jiun
    • Journal of Ginseng Research
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    • v.45 no.6
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    • pp.654-664
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    • 2021
  • Background: Ginsenoside Rg3, isolated from Panax ginseng, has anti-inflammatory and anti-tumor activities. It is known to reduce inflammation in acute lung injury in mice, and to reduce the expression of inflammatory cytokines and COX-2 in human asthmatic airway epithelium. In this study, we attempted to determine whether ginsenoside Rg3 inhibits airway inflammation, oxidative stress, and airway hyperresponsiveness (AHR) in the lungs of asthmatic mice. We also investigated its effects on oxidative stress and the inflammatory response in tracheal epithelial cells. Methods: Asthma symptoms were induced in female BALB/c mice sensitized with ovalbumin (OVA). Mice were divided into five groups: normal controls, OVA-induced asthmatic controls, and asthmatic mice treated with ginsenoside Rg3 or prednisolone by intraperitoneal injection. Inflammatory BEAS-2B cells (human tracheal epithelial cells) treated with ginsenoside Rg3 to investigate its effects on inflammatory cytokines and oxidative responses. Results: Ginsenoside Rg3 treatment significantly reduced eosinophil infiltration, oxidative responses, airway inflammation, and AHR in the lungs of asthmatic mice. Ginsenoside Rg3 reduced Th2 cytokine and chemokine levels in bronchoalveolar lavage fluids and lung. Inflammatory BEAS-2B cells treated with ginsenoside Rg3 reduced the eotaxin and pro-inflammatory cytokine expressions, and monocyte adherence to BEAS-2B cells was significantly reduced as a result of decreased ICAM-1 expression. Furthermore, ginsenoside Rg3 reduced the expression of reactive oxygen species in inflammatory BEAS-2B cells. Conclusion: Ginsenoside Rg3 is a potential immunomodulator that can ameliorate pathological features of asthma by decreasing oxidative stress and inflammation

Immune-Enhancing Activity of Wild Simulated Ginseng through TRL2/4-Dependent Activation of MAPK, NF-κB and PI3K/AKT Pathways (산양삼의 TRL2/4 의존성 MAPK, NF-κB 및 PI3K/AKT 신호전달 활성화를 통한 면역증진활성)

  • Jin Boo Jeong
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2020.08a
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    • pp.88-88
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    • 2020
  • Ginseng (Panax ginseng Meyer) is a very well-known traditional herbal medicine that has long been used to enhance the body's immunity. Because it is a type of ginseng, it is believed that wild simulated ginseng (WSG) also has immune-enhancing activity. However, study on the immune-enhancing activity of WSG is quite insufficient compared to ginseng. In this study, we evaluated immune-enhancing activity of WSG through macrophage activation to provide a scientific basis for the immune enhancing activity of WSG. WSG increased the production of immunomodulators such as NO, iNOS, COX-2, IL-1β, IL-6 and TNF-α and activated phagocytosis in mouse macrophages RAW264.7 cells. Inhibition of TLR2 and TLR4 reduced the production of immunomodulators induced by WSG. WSG activated MAPK, NF-κB and PI3K/AKT signaling pathways, and inhibition of such signaling activation blocked WSG-mediated production of immunomodulators. In addition, activation of MAPK, NF-κB and PI3K/AKT signaling pathways by WSG was reversed by TLR2 or TLR4 inhibition. Based on the results of this study, WSG is thought to activate macrophages through the production of immunomodulators and phagocytosis activation through TLR2/4-dependent MAPK, NF-κB and PI3K/AKT signaling pathways. Therefore, it is thought that WSG have the potential to be used as an agent for enhancing immunity.

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Analysis of Major Constituents of an Ethanol Extract of Platycodon Grandiflorum Leaves and Protective Effects on Inflammation in Murine Macrophage and Human Lung Carcinoma Cells (도라지 잎 에탄올 추출물의 주요 성분 분석 및 마우스 대식세포와 인체 폐암세포에서 항염효과)

  • Jung Min Lee;Byeong Jun Bae;Jee-Lim Choi;Young-Shin Chung
    • The Korean Journal of Food And Nutrition
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    • v.37 no.2
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    • pp.110-122
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    • 2024
  • This study investigated major constituents and anti-inflammatory effects of an ethanol extract of Platycodon grandiflorum leaves. Through HPLC analysis, chlorogenic acid and luteolin-7-O-glucoside were identified as predominant constituents in the ethanol extract. Their anti-inflammatory effects were evaluated using murine macrophage (RAW 264.7 cells) and human lung carcinoma cells (NCI-H292 & A549). The ethanol extract significantly (p<0.01) inhibited the production of nitrite, interleukin-6 (IL-6), and prostaglandin E2 (PGE2) induced by lipopolysaccharide (LPS) in RAW 264.7 cells. Furthermore, the ethanol extract suppressed the expression of cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) proteins in RAW 264.7 cells stimulated with LPS. In NCI-H292 and A549 cells, treatment with the ethanol extract significantly (p<0.05) decreased levels of pro-inflammatory cytokines IL-6 and IL-8 induced by IL-1β. The phosphorylation of ERK rather than JNK in the mitogen-activated protein kinase signaling pathway was observed to be a more important mediator in the down-regulation of pro-inflammatory cytokines in NCI-H292 cells. These findings suggest that the ethanol extract of Platycodon grandiflorum leaves containing luteolin-7-O-glucoside exhibits promising anti-inflammatory properties.

Association between Antacid Exposure and Risk of Interstitial Lung Diseases

  • Soohyun Bae;Gjustina Loloci;Dong Yoon Lee;Hye Jin Jang;Jihyeon Jeong;Won-Il Choi
    • Tuberculosis and Respiratory Diseases
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    • v.87 no.2
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    • pp.185-193
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    • 2024
  • Background: The mechanisms leading to lung fibrosis are still under investigation. This study aimed to demonstrate whether antacids could prevent the development of interstitial lung disease (ILD). Methods: This population-based longitudinal cohort study was conducted between January 2006 and December 2010 in South Korea. Eligible subjects were ≥40 years of age, exposed to proton pump inhibitors (PPI)±histamine-2 receptor antagonists (H-2 blockers) or H-2 blockers only, and had no history of ILD between 2004 and 2005. Exposure to antacids was defined as the administration of either PPI or H-2 receptor antagonists for >14 days, whereas underexposure was defined as antacid treatment administered for less than 14 days. Newly developed ILDs, including idiopathic pulmonary fibrosis (IPF), were counted during the 5-year observation period. The association between antacid exposure and ILD development was evaluated using adjusted Cox regression models with variables, such as age, sex, smoking history, and comorbidities. Results: The incidence rates of ILD with/without antacid use were 43.2 and 33.8/100,000 person-years, respectively and those of IPF were 14.9 and 22.9/100,000 person-years, respectively. In multivariable analysis, exposure to antacid before the diagnosis of ILD was independently associated with a reduced development of ILD (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.45 to 0.71; p<0.001), while antacid exposure was not associated with development of IPF (HR, 0.88; 95% CI, 0.72 to 1.09; p=0.06). Conclusion: Antacid exposure may be independently associated with a decreased risk of ILD development.

Anti-inflammatory Effects of Rebaudioside A in LPS-stimulated RAW264.7 Macrophage Cells (LPS에 의해 자극된 RAW264.7 대식세포에서 Rebaudioside A의 항염 효과)

  • Cho, Uk Min;Hwang, Hyung Seo
    • Journal of the Society of Cosmetic Scientists of Korea
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    • v.43 no.2
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    • pp.157-164
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    • 2017
  • Stevia (Stevia rebaudiana) is a perennial plant of the genus Stevia, originated in South America. It stores many forms of glycosides, mainly stevioside and rebaudioside A, in which steviol is the basic structure. Steviol glycosides, widely used as sweeteners, are superior to sugar in sweetness. Recently, it has been reported that steviol glycosides are involved not only in the skin whitening and anti-inflammatory effect but also in enhancing skin barrier function through tight junction regulation. Thus, we examined anti-inflammatory effect of rebaudioside A and tried to identify its potential for improving atopic dermatitis as cosmetic ingredients. To investigate the anti-inflammatory effect, cell viability and mRNA expression level of inflammation-related cytokines were measured using mouse macrophage RAW264.7 cells. Cell counting kit 8 (CCK-8) assay was carried out to measure cell viability and the maximum concentration without cytotoxicity was set to $250{\mu}M$. A quantitative real-time RT-PCR method was used for the study of the inflammatory suppression of rebaudioside A. Rebaudioside A inhibited expression of inducible nitric oxide synthase (iNOS) up to 47% and COX-2 up to 41% compared to LPS treated condition. NO synthesis was decreased by rebaudioside A. Also, mRNA expression of interleukin (IL)-$1{\alpha}$, IL-$1{\beta}$ and IL-6 in LPS-stimulated RAW264.7 cells was decreased to 40%, 45% and 59%, respectively, as a concentration-dependent manner. In conclusion, rebaudioside A inhibited the inflammatory response by regulation of cytokine gene expression. From these results, we expect that steviol glycoside, such as rebaudioside A, can be used as a material for improving atopic dermatitis in the future.

Inhibitory Effect of Protaetiamycine 9 Derived from Protaetia brevitarsis seulensis Larvae on LPS-mediated Inflammation in RAW264.7 Cells (LPS로 자극한 RAW264.7 대식세포에서 흰점박이꽃무지 유충 유래 Protaetiamycine 9의 항염증 효과)

  • Choi, Ra-Yeong;Seo, Minchul;Lee, Joon Ha;Kim, In-Woo;Kim, Mi-Ae;Hwang, Jae-Sam
    • Journal of Life Science
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    • v.31 no.11
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    • pp.987-994
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    • 2021
  • Our previous studies have reported that antimicrobial peptides (AMPs) derived from the larvae of white-spotted flower chafer (Protaetia brevitarsis seulensis) exert anti-inflammatory and neuroprotective activities. This study explored the anti-inflammatory effects of protaetiamycine 9 (CVLKKAYFLTNLKLRG-NH2), a novel AMP, derived from P. b. seulensis against lipopolysaccharide (LPS)-mediated inflammatory response in RAW264.7 macrophage cells. Protaetiamycine 9 (25, 50, 75, and 100 ㎍/ml) did not cause cytotoxic effects against RAW264.7 cells. The RAW264.7 cells were pre-treated with various concentrations of protaetiamycine 9 (25-100 ㎍/ml) for 1 hr and then exposed to LPS (100 ng/ml) for 24 hr. Protaetiamycine 9 treatments decreased the LPS-induced secretion of inflammatory mediators, such as nitric oxide (NO), in a dose-dependent manner. Protaetiamycine 9 (25-100 ㎍/ml) effectively downregulated the LPS-induced increase in mRNA and the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), which are involved in the production of inflammatory mediators. Protaetiamycine 9 also suppressed the production and gene expression of pro-inflammatory cytokines, including interleukin (IL)-6 and IL-1β, compared to the presence of LPS alone. Furthermore, protaetiamycine 9 inhibited the degradation of inhibitory kappa B alpha (IκB-α) and the phosphorylation of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. In conclusion, these results suggest that protaetiamycine 9 exhibits LPS-mediated inflammatory responses by blocking IκB-α degradation and MAPK phosphorylation.

Anticolitic Effect of the Rhizome Mixture of Anemarrhena asphodeloides and Coptidis chinensis (AC-mix) in Mice

  • Jang, Se-Eun;Jeong, Jin-Ju;Hyam, Supriya R.;Han, Myung Joo;Kim, Dong-Hyun
    • Biomolecules & Therapeutics
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    • v.21 no.5
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    • pp.398-404
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    • 2013
  • During a screening program to search the anticolitic herbal medicines, 80% ethanol extract of the rhizome of Anemarrhena asphodeloides (AA) was found to potently inhibit the expression of proinflammatory cytokines TNF-${\alpha}$ and IL-1${\beta}$, as well as the activation of NF-${\kappa}B$ in LPS-stimulated colonic macrophages, followed by that of the rhizome of C. chinensis (CC). AA also potently inhibited TNBS-induced colitic markers, shortening of the colon and increase of macroscopic score, myeloperoxidase activity, TNF-${\alpha}$, IL-1${\beta}$, and IL-6, in mice. The synergistic effect of CC against the anticolitic effect of AA was investigated. CC synergistically inhibited the anticolitic effect of AA. AC-mix (AA+CC, 1:1) potently inhibited them. AC-mix also inhibited the activation of NF-${\kappa}B$, as well as the expression of TNF-${\alpha}$, IL-1${\beta}$, IL-6, iNOS and COX-2. The effects of AC-mix against oxazolone-induced colitis were investigated in mice. AC-mix also potently inhibited oxazolone-induced inflammatory markers, colon shortening, macroscopic score, myeloperoxidase activity, NF-${\kappa}B$ activation and proinflammatory cytokines. Overall, the anti-colitic effect of AC-mix was superior to that of mesalazine. Based on these findings, AC-mix may improve colitis by inhibiting NF-${\kappa}B$ activation.

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.

Survival Rate of Extrahepatic Cholangiocarcinoma Patients after Surgical Treatment in Thailand

  • Pattanathien, Pisit;Khuntikeo, Narong;Promthet, Supannee;Kamsa-ard, Supot
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.1
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    • pp.321-324
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    • 2013
  • Background: Intra- and extrahepatic cholangiocarcinoma (CCA) is the most common cancer in Thailand, especially in the northeast region. Most extrahepatic CCA patients consult a doctor at a late stage. Surgery is still the best treatment. Objectives: The aim of this study was to evaluate survival rates and factors affecting survival in extrahepatic CCA patients following surgery at Srinagarind Hospital, Khon Kaen University, Thailand. Materials and Methods: A retrospective cohort study was conducted with 58 patients who were diagnosed and treated by surgical resection by the same surgeon at Srinagarind Hospital between 2005 and 2009. The patients were followed up until death or the end of the study (31 December, 2011). Survival rates were calculated by the Kaplan-Meier method, and the Cox proportional hazard model was used to identify independent prognostic factors. Results: The total follow-up time was 1,215 person-months, and the mortality rate was 50 per 100 person-years. The cumulative 1-, 3-, and 5-year survival rates were 62.1%, 21.7% and 10.8%, respectively. The median survival time after resection was 15 months. After adjusting for age, gender, lymph node metastasis and histological type, resection margin remained as a statistically significant prognostic factor for survival following surgery. A positive resection margin was associated with a 2.3-fold higher mortality rate than a negative margin. Conclusions: Resection margins are important prognostic factors affecting survival of extrahepatic CCA patients after surgery. A negative resection margin can reduce the mortality rate by 56%.