• 제목/요약/키워드: Inflammation biomarkers

검색결과 118건 처리시간 0.026초

떫은감 진피 복합추출물의 급성 역류성 식도염 개선 효과 (Improving Effects on Rats with Reflux Esophagitis Treated with Combined Extract of Young persimmon fruit and Citrus peel)

  • 권오준;이아름;노성수
    • 대한본초학회지
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    • 제31권1호
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    • pp.25-31
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    • 2016
  • Objectives : The present study was conducted to evaluate protective effects of Combined Extract of young persimmon fruit and citrus peel (PCM) in Reflux Esophagitis(RE) rats.Methods : Twenty-four Sprague-Dawley (SD) rats were divided four groups and each group had six rats ; Normal group, RE control group, RE group treated PCM 50 ,100 mg/kg body weight group. Reflux esophagitis was induced that tied the pylorus and fundus in SD rats stomach. PCM was administered at 50, 100 mg/kg body weight 2 hrs prior to induction of RE. After 6 hrs, the effects of PCM treated rats were compared with those of normal and control rats. We have performed an analysis such as pH of stomach secretion, oxidative stress biomarkers in serum, and western blot.Results : The increased esophageal mucosa damage by RE was markedly improved by PCM treatment in a dose-dependent manner. Also, the administration of PCM decreased the elevated serum reactive oxygen species (ROS) and peroxynitrite (ONOO-) in serum. The protein expressions of anti oxidant such as SOD, catalase, GPx exhibited down-regulation by PCM treatment in tissues. And, PCM effectively reduce inflammatory cytokines such as inflammation-related proteins cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in RE rats. In addition, NFκB and p-IκBɑ were decreased in PCM-adiministrated RE rats. But there was no difference on stomach secretion pH between reflux esophagitis rats and PCM administration rat group.Conclusions : In conclusion, administration of PCM (50, 100 mg/kg body weight) made esophagus have less inflammation and injury by decreased NFκB path way. These findings suggest that PCM could have Improving effects on reflux esophagitis.

Anti-Inflammatory Effect of Asterias amurensis Fatty Acids through NF-κB and MAPK Pathways against LPS-Stimulated RAW264.7 Cells

  • Monmai, Chaiwat;Go, Seok Hyeon;Shin, Il-sik;You, SangGuan;Kim, Dae-ok;Kang, SeokBeom;Park, Woo Jung
    • Journal of Microbiology and Biotechnology
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    • 제28권10호
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    • pp.1635-1644
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    • 2018
  • Asterias amurensis (starfish) is a marine organism that is harmful to the fishing industry, but is also a potential source of functional materials. The present study was conducted to analyze the profiles of fatty acids extracted from A. amurensis tissues and their anti-inflammatory effects on RAW264.7 macrophage cells. In different tissues, the component ratios of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids differed; particularly, polyunsaturated fatty acids such as dihomo-gamma-linolenic acid (20:3n-6) and eicosapentaenoic acid (20:5n-3) were considerably different. In lipopolysaccharide-stimulated RAW264.7 cells, fatty acids from A. amurensis skin, gonads, and digestive glands exhibited anti-inflammatory activities by reducing nitric oxide production and inducing nitric oxide synthase gene expression. Asterias amurensis fatty acids effectively suppressed the expression of inflammatory cytokines such as tumor necrosis $factor-{\alpha}$, interleukin-$1{\beta}$, and interleukin-6 in lipopolysaccharide-stimulated cells. Cyclooxygenase-2 and prostaglandin $E_2$, which are critical inflammation biomarkers, were also significantly suppressed. Furthermore, A. amurensis fatty acids reduced the phosphorylation of nuclear $factor-{\kappa}B$ p-65, p38, extracellular signal-related kinase 1/2, and c-Jun N-terminal kinase, indicating that these fatty acids ameliorated inflammation through the nuclear $factor-{\kappa}B$ and mitogen-activated protein kinase pathways. These results provide insight into the anti-inflammatory mechanism of A. amurensis fatty acids on immune cells and suggest that the species is a potential source of anti-inflammatory molecules.

High-fat Diet Accelerates Intestinal Tumorigenesis Through Disrupting Intestinal Cell Membrane Integrity

  • Park, Mi-Young;Kim, Min Young;Seo, Young Rok;Kim, Jong-Sang;Sung, Mi-Kyung
    • Journal of Cancer Prevention
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    • 제21권2호
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    • pp.95-103
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    • 2016
  • Background: Excess energy supply induces chronic low-grade inflammation in association with oxidative stress in various tissues including intestinal epithelium. The objective of this study was to investigate the effect of high-fat diet (HFD) on intestinal cell membrane integrity and intestinal tumorigenesis in $Apc^{Min/+}$ mice. Methods: Mice were fed with either normal diet (ND) or HFD for 12 weeks. The number of intestinal tumors were counted and biomarkers of endotoxemia, oxidative stress, and inflammation were determined. Changes in intestinal integrity was measured by fluorescein isothiocyanate (FITC)-dextran penetration and membrane gap junction protein expression. Results: HFD group had significantly higher number of tumors compared to ND group (P < 0.05). Blood total antioxidant capacity was lower in HFD group, while colonic 8-hydroxy-2'-deoxyguanosine level, a marker of oxidative damage, was higher in HFD group compared to that of ND group (P < 0.05). The penetration of FITC-dextran was substantially increased in HFD group (P < 0.05) while the expressions of membrane gap junction proteins including zonula occludens-1, claudin-1, and occludin were lower in HFD group (P < 0.05) compared to those in ND group. Serum concentration of lipopolysaccharide (LPS) receptor (CD14) and colonic toll-like receptor 4 (a LPS receptor) mRNA expression were significantly higher in HFD group than in ND group (P < 0.05), suggesting that significant endotoxemia may occur in HFD group due to the increased membrane permeability. Serum interleukin-6 concentration and myeloperoxidase activity were also higher in HFD group compared to those of ND group (P < 0.05). Conclusions: HFD increases oxidative stress disrupting intestinal gap junction proteins, thereby accelerating membrane permeability endotoxemia, inflammation, and intestinal tumorigenesis.

Development of a food-based index of dietary inflammatory potential for Koreans and its relationship with metabolic syndrome

  • Na, Woori;Yu, Tae Yang;Sohn, Cheongmin
    • Nutrition Research and Practice
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    • 제13권2호
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    • pp.150-158
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    • 2019
  • BACKGROUND/OBJECTIVES: Inflammation is known to be a risk factor for metabolic diseases. This study aimed to develop a Food-based Index of Dietary Inflammatory Potential (FBDI) and examine its association with metabolic biomarkers. SUBJECTS/METHODS: This study analyzed the raw data from the 2012-2014 Korean Genome and Epidemiology Study data of 17,771 people. To analyze the relationship between foods consumed by Koreans and inflammation, we conducted a correlation analysis between 51 food groups and hs-CRP levels. The FBDI was developed from 17 food groups selected by multiple regression method. We examined whether FBDI was associated with metabolic markers (waist circumference, blood pressure, fasting glucose, triglyceride, and HDL-cholesterol) in the 6th Korea National Health and Nutrition Examination Survey (KNHANES). We used binary logistic regression analysis to examine the association. RESULTS: The FBDI model included seven of the anti-inflammatory food groups and three of the pro-inflammatory food groups. The FBDI formula was calculated by multiplying the intake of food group by ${\beta}$-coefficients derived from the multiple regression model based on the correlation analysis. The FBDI was significantly associated with waist circumference (P < 0.001), blood pressure (P < 0.001), triglyceride level (P < 0.001), and HDL-cholesterol (P < 0.001) level among adults aged 20-64 years in the KNHANES. The prevalence of metabolic syndrome was 2.618 times higher in the group with the highest FBDI than in the group with the lowest one (95% confidence interval: 1.778-3.856, P for trend < 0.001). CONCLUSIONS: This study established an FBDI reflecting food intake patterns of Koreans, which showed a significant relationship with the prevalence of metabolic syndrome.

Silymarin과 작약감초탕 병용투여의 C57BL/6 마우스 간조직 지질축적 및 염증 억제효과 (Combined Treatment of Silymarin and Jakyakgamcho-tang Suppresses Hepatic Lipid Accumulation and Inflammation in C57BL/6 Mice)

  • 최정원;조수정;신미래;박해진
    • 대한본초학회지
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    • 제37권5호
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    • pp.17-26
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    • 2022
  • Objective : The aim of the present study is to examine hepatic lipid-lowering and anti-inflammatory effects of silymarin combined with Jakyakgamcho-tang on non-alcoholic fatty liver disease in a high fat diet-induced obese mice model. Methods : C57BL/6 mice were divided into four dietary groups: (1) Normal, (2) Control (60% high-fat diet), (3) Control + silymarin 50 mg/kg/day (Silymarin), (4) Control + Silymarin 50 mg/kg/day + Jakyakgamcho-tang 100 mg/kg/day (SPG). After 12 weeks administration, mice were sacrificed and lipids and inflammation-related biomarkers were analyzed liver and plasma. Results : Silymarin and SPG treatments significantly lowered body and liver weights compared to the Control. Serumlipids (triglyceride (TG), total cholesterol) and pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin 1𝛽, and IL-6) concentrations were significantly lowered in the Silymarin and SPG groups than the Control group. Silymarin and SPG treatments suppressed hepatic TG level and hepatic lipid droplets compared to the Control. Theses two treatments significantly increased hepatic kinase B1 and AMP-activated protein kinase protein levels, and significantly decreased hepatic key lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase and stearyl coenzyme A desaturase 1) protein levels than the Control. SPG also significantly increased hepatic fatty acid oxidation-related protein (peroxisome proliferator-activated receptor alpha and uncoupling protein 2) levels than the Control. Conclusions: Silymarin and SPG suppressed hepatic lipid accumulation by regulating hepatic protein expression, and lowered blood pro-inflammatory cytokines concentrations though the synergic effect of silymarin and Jakyakgamchotang was not clear.

기혈소통환(氣血疏通丸)이 Monosodium iodoacetate로 골관절염(骨關節炎)을 유도(誘導)한 랫드에 미치는 영향(影響) (Effects of gihyeolsotong-hwan on monosodium iodoacetate-induced osteoarthritis in rats)

  • 허문강;김순근;최학주;김동희
    • 대한본초학회지
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    • 제33권3호
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    • pp.45-53
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    • 2018
  • Objectives : In cases of osteoarthritis, the hypofunction of the cartilage and joint leads to a limited range of joint motion, swelling, and pain, which is generally treated using pharmaceutical drugs (e.g., anti-inflammatory agents, cartilage protectants, and nonsteroidal anti-inflammatory drugs) or replacement arthroplasty. However, long-term drug treatment is associated with adverse effects on the gastrointestinal systems. The present study aimed to evaluate the ability of Giheolsotong-hwan to treat of osteoarthritis symptoms in the MIA-induced rat model based on histological analysis, and factors that are associated with inflammation and bone mineral metabolism. Methods : Giheolsotong-hwan was administered orally at doses of 200 mg/kg/day or 400 mg/kg/day for 2 weeks before direct injection of monosodium iodoacetate ($3mg/50{\mu}{\ell}$ of 0.9% saline) into the intra-articular space of the rats' right knee. The rats subsequently received the same doses of oral Giheolsotong-hwan for another 4 weeks. We evaluated the treatment effects based on serum biomarkers and histopathological analysis of the knee joints. Results : Compared to those in control rats, the Giheolsotong-hwan treatments significantly decreased the serum concentration of inflammation factors (i.e., $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, $PGE_2$, and $LTB_4$), and bone degrade factors (i.e., MMP-9, CTX-II, and COMP). In addition, the Giheolsotong-hwan treatments significantly increased the concentration of glycosaminoglycans of bone defence factors, but no chage the TIMP-1. Furthermore, the Giheolsotong-hwan treatments effectively preserved the knee cartilage and proteoglycan. Conclusion : The results indicate that Giheolsotong-hwan treated osteoarthritis symptoms. Thus, Giheolsotong-hwan may be a novel oriental therapeutic option for the management of osteoarthritis.

Mollugin-mediated Inhibition of Proinflammatory Biomarkers in Lipopolysaccharide-stimulated RAW264.7 Cells

  • Kim, Jin-Kyung;Park, Geun-Mook;Jun, Jong-Gab
    • 대한의생명과학회지
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    • 제18권4호
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    • pp.338-344
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    • 2012
  • Mollugin is the active compound of Rubia cordifolia, a well known herb widely used in alternative medicines for the treatment of various inflammatory diseases including arthritis and uteritis. In the present study, we investigated the anti-inflammatory effects of mollugin in lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophage cells. Treatment with mollugin significantly inhibited LPS-induced release of nitric oxide, prostaglandin $E_2$, and inflammatory cytokines, such as tumor necrosis factor-${\alpha}$ and interleukin-6. In addition, mollugin suppressed LPS-induced nuclear factor-kappa B (NF-${\kappa}B$) transcriptional activity. These results suggest that mollugin inhibits LPS-induced expression of inflammatory molecules via NF-${\kappa}B$, at least in part, and indicate the potential value of mollugin as a valuable new drug candidate for the treatment of various inflammatory diseases.

Receptor for Advanced Glycation Endproducts (RAGE), Its Ligands, and Soluble RAGE: Potential Biomarkers for Diagnosis and Therapeutic Targets for Human Renal Diseases

  • Lee, Eun Ji;Park, Jong Hoon
    • Genomics & Informatics
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    • 제11권4호
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    • pp.224-229
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    • 2013
  • Receptor for advanced glycation endproducts (RAGE) is a multi-ligand receptor that is able to bind several different ligands, including advanced glycation endproducts, high-mobility group protein (B)1 (HMGB1), S-100 calcium-binding protein, amyloid-${\beta}$-protein, Mac-1, and phosphatidylserine. Its interaction is engaged in critical cellular processes, such as inflammation, proliferation, apoptosis, autophagy, and migration, and dysregulation of RAGE and its ligands leads to the development of numerous human diseases. In this review, we summarize the signaling pathways regulated by RAGE and its ligands identified up to date and demonstrate the effects of hyper-activation of RAGE signals on human diseases, focused mainly on renal disorders. Finally, we propose that RAGE and its ligands are the potential targets for the diagnosis, monitoring, and treatment of numerous renal diseases.

Physical Activity and its Relation to Cancer Risk: Updating the Evidence

  • Kruk, Joanna;Czerniak, Urszula
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권7호
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    • pp.3993-4003
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    • 2013
  • Scientific evidence for the primary prevention of cancer caused by physical activity of regular moderate-intensity or greater is rapidly accumulating in this field. About 300 epidemiologic studies on the association between physical activity and cancer risk have been conducted worldwide. The objectives of this paper were three-fold: (i) to describe briefly the components of physical activity and its quantification; (ii) to summarize the most important conclusions available from comprehensive reports, and reviews of the epidemiologic individual and intervention studies on a role physical activity in cancer prevention; (iii) to present proposed biological mechanisms accounting for effects of activity on cancer risk. The evidence of causal linked physical activity and cancer risk is found to be strong for colon cancer - convincing; weaker for postmenopausal breast and endometrium cancers - probable; and limited suggestive for premenopausal breast, lung, prostate, ovary, gastric and pancreatic cancers. The average risk reductions were reported to be 20-30%. The protective effects of physical activity on cancer risk are hypothesized to be through multiple interrelated pathways: decrease in adiposity, decrease in sexual and metabolic hormones, changes in biomarkers and insulin resistance, improvement of immune function, and reduction of inflammation. As there are several gaps in the literature for associations between activity and cancer risk, additional studies are needed. Future research should include studies dealing with limitations in precise estimates of physical activity and of a lack of consensus on what defines sedentary behavior of individuals and those linked with the proposed biomarkers to cancer risk and controlled exercise intervention trials.

The Effect of Green Coffee Supplementation on Lipid Profile, Glycemic Indices, Inflammatory Biomarkers and Anthropometric Indices in Iranian Women With Polycystic Ovary Syndrome: A Randomized Clinical Trial

  • Mehrnoush Meshkani;Ahmad Saedisomeolia;Mirsaeed Yekaninejad;Seyed Ahmad Mousavi;Azam Ildarabadi;Marzieh Vahid-Dastjerdi
    • Clinical Nutrition Research
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    • 제11권4호
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    • pp.241-254
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    • 2022
  • Polycystic ovary syndrome (PCOS) is a heterogeneous clinical syndrome. Recent studies examine different strategies to modulate its related complications. Chlorogenic acid, as a bioactive component of green coffee (GC), is known to have great health benefits. The present study aimed to determine the effect of GC on lipid profile, glycemic indices, and inflammatory biomarkers. Forty-four PCOS patients were enrolled in this randomized clinical trial of whom 34 have completed the study protocol. The intervention group (n = 17) received 400 mg of GC supplements, while the placebo group (n = 17) received the same amount of starch for six weeks. Then, glycemic indices, lipid profiles, and inflammatory parameters were measured. After the intervention period, no significant difference was shown in fasting blood sugar, insulin level, Homeostasis model assessment of insulin resistance index, low-density lipoprotein, high-density lipoprotein, Interleukin 6 or 10 between supplementation and placebo groups. However, cholesterol and triglyceride serum levels decreased significantly in the intervention group (p < 0.05). This research confirmed that GC supplements might improve some lipid profiles in women with PCOS. However, more detailed studies with larger sample sizes are required to prove the effectiveness of this supplement.