• Nutrition Research and Practice
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• v.13 no.1
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• pp.3-10
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• 2019

BACKGROUND/OBJECTIVES: The $NAD^+$ precursor nicotinamide riboside (NR) is a type of vitamin $B_3$ found in cow's milk and yeast-containing food products such as beer. Recent studies suggested that NR prevents hearing loss, high-fat diet-induced obesity, Alzheimer's disease, and mitochondrial myopathy. The objective of this study was to investigate the effects of NR on inflammation and mitochondrial biogenesis in AML12 mouse hepatocytes. MATERIALS/METHODS: A subset of hepatocytes was treated with palmitic acid (PA; $250{\mu}M$) for 48 h to induce hepatocyte steatosis. The hepatocytes were treated with NR ($10{\mu}M$ and 10 mM) for 24 h with and without PA. The cell viability and the levels of sirtuins, inflammatory markers, and mitochondrial markers were analyzed. RESULTS: Cytotoxicity of NR was examined by PrestoBlue assay. Exposure to NR had no effect on cell viability or morphology. Gene expression of sirtuin 1 (Sirt1) and Sirt3 was significantly upregulated by NR in PA-treated hepatocytes. However, Sirt1 activities were increased in hepatocytes treated with low-dose NR. Hepatic pro-inflammatory markers including tumor necrosis factor-alpha and interleukin-6 were decreased in NR-treated cells. NR upregulated anti-inflammatory molecule adiponectin, and, tended to down-regulate hepatokine fetuin-A in PA-treated hepatocytes, suggesting its inverse regulation on these cytokines. NR increased levels of mitochondrial markers including peroxisome proliferator-activated receptor ${\gamma}$ coactivator-$1{\alpha}$, carnitine palmitoyltransferase 1, uncoupling protein 2, transcription factor A, mitochondrial and mitochondrial DNA in PA-treated hepatocytes. CONCLUSIONS: These data demonstrated that NR attenuated hepatic inflammation and increased levels of mitochondrial markers in hepatocytes.

• Clinical Psychopharmacology and Neuroscience
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• v.16 no.4
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• pp.422-433
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• 2018

Objective: Neuropsychiatric manifestations like depression and cognitive dysfunction commonly occur in inflammatory bowel disease (IBD). In the context of the brain-gut axis model, colitis can lead to alteration of brain function in a bottom-up manner. Here, the changes in the response of the hypothalamic-pituitary-adrenal axis and inflammation-related markers in the brain in colitis were studied. Methods: Dextran sodium sulfate (DSS) was used to generate a mouse model of colitis. Mice were treated with DSS for 3 or 7 days and sacrificed. We analyzed the gene expression of brain-derived neurotrophic factor (BDNF), cyclooxygenase 2 (COX-2), and glial fibrillary acidic protein (GFAP), and the expression of GFAP, in the hippocampus, hypothalamus, and amygdala. Additionally, the levels of C-reactive protein (CRP) and serum cortisol/corticosterone were measured. Results: Alteration of inflammatory-related markers varied depending on the brain region and exposure time. In the hippocampus, COX-2 mRNA, GFAP mRNA, and GFAP expression were upregulated during exposure to DSS. However, in the hypothalamus, COX-2 mRNA was upregulated only 3 days after treatment. In the amygdala, BDNF and COX-2 mRNAs were downregulated. CRP and corticosterone expression increased with DSS treatment at day 7. Conclusion: IBD could lead to neuroinflammation in a bottom-up manner, and this effect varied according to brain region. Stress-related hormones and serum inflammatory markers, such as CRP, were upregulated from the third day of DSS treatment. Therefore, early and active intervention is required to prevent psychological and behavioral changes caused by IBD, and region-specific studies can help understand the precise mechanisms by which IBD affects the brain.

• Journal of the Korean Society of Physical Medicine
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• v.14 no.1
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• pp.63-73
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• 2019

PURPOSE: This study examined the effects of cardiopulmonary physiotherapy on the cardiopulmonary function, metabolism, inflammatory markers, and quality of life in patients with coronary artery disease who underwent percutaneous coronary intervention (PCI). METHODS: Electronic bibliographic databases of a regional information sharing system (RISS) and PubMed were searched to identify studies with randomized and non-randomized controlled trials. As the final outcome, 320 publications were identified and 18 studies met the inclusion and exclusion criteria. All studies were assessed for the quality of study using Cochrane's risk of bias. RESULTS: Sixteen studies met the inclusion criteria, in which meta-analysis had been conducted to examine the effectiveness of cardiopulmonary physiotherapy on the cardiopulmonary function, metabolism, inflammatory markers, and quality of life in patients undergoing PCI. Meta-analysis based on a random effect model showed that the cardiopulmonary physiotherapy was beneficial in improving the cardiopulmonary function, metabolism, inflammatory markers, and quality of life. In particular, there was a significant effect on the peak oxygen uptake (effect size 5.30%; 95% confidence interval 3.62~6.97). Cardiopulmonary physiotherapy for a during period of 6 weeks or more was effective in significantly improving the cardiopulmonary function and metabolism function in a subgroup analysis, but cardiopulmonary physiotherapy for less than 6 weeks was not effective. CONCLUSION: Cardiopulmonary physiotherapy has positive effects on the cardiopulmonary function, metabolism, inflammatory markers, and quality of life in patients undergoing PCI.

• Biomedical Science Letters
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• v.22 no.4
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• pp.220-226
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• 2016

Hypertriglyceridemia induces atherosclerosis and accordingly is a major causative factor in cardiovascular diseases. Macrophages that develop into foam cells are a crucial component in the development of atherosclerosis. Monocytes can be differentiated into M1 or M2 macrophages. M1 macrophages promote inflammatory responses, whereas M2 macrophages exhibit anti-inflammatory activity. Recently, we found that triglyceride (TG)-treated THP-1 monocytes express a variety of macrophage-specific surface markers, indicating that TG treatment could trigger the differentiation of monocytes into macrophages. In this study, we investigated whether TG-induced macrophages express the M1 or the M2 macrophage phenotype. THP-1 cells were treated with various concentrations of TG for different times and the expression of M1- and M2-specific markers was evaluated by RT-PCR. We found increased expression of M1 markers (CD40, CD80, and CD86) in TG-treated THP-1 cells in a TG dose- and time-dependent manner. The expression of M2 markers (CD163, CD200R, and CD206) showed variable responses to TG treatment. Taken together, our results indicate that TG treatment triggers the differentiation of monocytes into M1 macrophages, rather than into M2 macrophages, suggesting that TG contributes to pro-inflammatory responses.

• Journal of the East Asian Society of Dietary Life
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• v.21 no.5
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• pp.637-648
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• 2011

This study was designed to investigate the relationship between the nutrient intakes, antioxidants, and inflammatory markers of overweight and obese adults (46 females and 16 males) in Yeongdong area. The study was conducted through questionnaires, anthropometric checkups, 2-day 24 hr recalls and blood biomarker analyses. Body fat was significantly higher in women compared to men. Diastolic blood pressure (DBP) and systolic blood pressure (SBP) were significantly higher in men compared to women. There were no significant differences in height, weight, body mass index, and waist size among the two groups. The intake of nutrients was significantly higher in men compared to women. Ferric reducing ability plasma (FRAP) was significantly higher in men compared to women. Body fat was positively associated with blood IL-6 and IL-8 levels. DBP was positively associated with FRAP. The intake of protein was negatively associated with IL-6 levels. The intake of carbohydrates was negatively associated with total antioxidant capacity (TAC). Prostaglandin E2 (PGE2) levels were negatively associated with TAC. These results suggest that antioxidant and inflammatory markers may be related to the body fat percentage and dietary intake in overweight and obese adults.

• Biomedical Science Letters
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• v.18 no.3
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• pp.237-243
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• 2012

This study was undertaken to know the effect of fat diet (for eight weeks) on changes of inflammatory markers [tumor necrosis factor (TNF-${\alpha}$) and prostaglandin $E_2$ ($PGE_2$)] and blood coagulation system [platelet aggregation function (PAF), prothrombin time (PT), activated partial thromboplastin time (aPTT)] in rats. Serum TNF-${\alpha}$, $PGE_2$, biochemical markers, PAF, PT, aPTT, and body weight were measured and compared between the control (normal diet-rats) and the fat group (fat diet-rats). The weights in the fat group were higher than those of the control group. TNF-${\alpha}$, $PGE_2$, glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatinine levels were greater in the fat group compared with the control group. The degree of platelet aggregation was lower, whereas PT and aPTT levels were longer in the fat group than in the control group. These findings have shown that fat diet may cause inflammatory response, diabetes, liver and renal dysfunction, and disturbances of fibrinolysis and coagulation system.

• Parasites, Hosts and Diseases
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• v.62 no.1
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• pp.30-41
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• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.3
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• pp.177-187
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• 2021

Metabolic syndrome (MBS) is a widespread disease that has strongly related to unhealthy diet and low physical activity, which initiate more serious conditions such as obesity, cardiovascular diseases and type 2 diabetes mellitus. This study aimed to examine the therapeutic effects of morin, as one of the flavonoids constituents, which widely exists in many herbs and fruits, against some metabolic and hepatic manifestations observed in MBS rats and the feasible related mechanisms. MBS was induced in rats by high fructose diet feeding for 12 weeks. Morin (30 mg/kg) was administered orally to both normal and MBS rats for 4 weeks. Liver tissues were used for determination of liver index, hepatic expression of glucose transporter 2 (GLUT2) as well as both inflammatory and fibrotic markers. The fat/muscle ratio, metabolic parameters, systolic blood pressure, and oxidative stress markers were also determined. Our data confirmed that the administration of morin in fructose diet rats significantly reduced the elevated systolic blood pressure. The altered levels of metabolic parameters such as blood glucose, serum insulin, serum lipid profile, and oxidative stress markers were also reversed approximately to the normal values. In addition, morin treatment decreased liver index, serum liver enzyme activities, and fat/muscle ratio. Furthermore, morin relatively up-regulated GLUT2 expression, however, down-regulated NF-κB, TNF-α, and TGF-β expressions in the hepatic tissues. Here, we revealed that morin has an exquisite effect against metabolic disorders in the experimental model through, at least in part, antioxidant, anti-inflammatory, and anti-fibrotic mechanisms.

• Clinical and Experimental Pediatrics
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• v.60 no.11
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• pp.359-364
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• 2017

Purpose: The risk of cardiovascular disease (CVD) has been shown to be associated with systemic inflammation in obese adults with metabolic syndrome (MetS). The aims of this study were to evaluate the prevalence of MetS and its relation to inflammatory markers in obese Thai children. Methods: A cross-sectional study was conducted. Children with history of endogenous obesity, chronic diseases, drug ingestion, and any acute illness within 2 weeks prior to enrollment were excluded. Their fasting blood glucose (FBG) levels, oral glucose tolerance tests, insulin, lipid profiles, and selected inflammatory markers, including interleukin-6, tumor necrosis factor-alpha, and high-sensitivity C-reactive protein (hs-CRP) levels, were tested. Results: In this study, 58 obese Thai children (female, 20; male, 38) with a mean body mass index z score of $5.1{\pm}2.2$ were enrolled. The prevalence of MetS and prediabetes was 31% and 17.2%, respectively. None of the children had diabetes. FBG levels, 2-hour glucose levels, and lipid profiles were not statistically different between those with and without MetS. However, obese children with MetS had higher insulin levels and homeostasis model assessment of insulin resistance values. Elevated hs-CRP levels were found in 69% of the cases, although it was not statistically different between the 2 groups. Conclusion: We described a substantial prevalence of MetS in Thai obese children. Regardless of MetS status, two-thirds of the obese children had elevated hs-CRP level, indicating subtle ongoing inflammatory process. This chronic inflammation feasibly predisposes them to CVD in the future, even in children without MetS.

• The Korea Journal of Herbology
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• v.35 no.2
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• pp.7-14
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• 2020

Objectives : Pyeongwi-san is widely used in Korean medicine for acute indigestion or gastrodynia. As a therapeutic agent for digestive diseases of modern people, in order to confirm the mechanism of Pyeongwi-san on digestive tract disease and the difference of therapeutic efficacy between its formulation, a comparative efficacy test was conducted on digestive tract disease animal model. Methods : For LPS enteritis animal model, male SD rats were intraorally treated with different formulation types of Pyeongwi-san, and then intraperitoneally administered LPS one hour later to induce enteritis. After 5 hours, blood was collected and TNFα, IL-1β, IL-6 and PGE2 were confirmed by ELISA. For acute gastritis animal model, male SD rats were intraorally treated with different formulation types of Pyeongwi-san according to the prescribed concentration, and then intraorally administered 60% ethanol and 150 mM HCl one hour later to induce acute gastritis. After 5 hours, blood was collected and TNFα,IL-6 were confirmed by ELISA. Results : In the LPS-administered enteritis animal model, Pyeongwi-san decreased TNFα, IL-1β, PGE2 and especially IL-6. Pyeongwi-san also decreased IL-6 in acute gastritis animal model. In addition, there was no significant difference in efficacy between the two formulations when compared with inflammatory markers. Conclusions : The efficacy of Pyeongwi-san was confirmed in the inflammatory markers related to digestive inflammatory diseases, and the efficay between two formulations of Pyeongwi-san was relatively similar. Further studies are needed to investigate the new applicability of Pyeongwi-san on different inflammatory diseases that have similar inflammation markers identified in this experiment.