• The Journal of the Korea Contents Association
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• v.16 no.7
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• pp.465-475
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• 2016

The incidence of inflammatory bowel disease(IBD) has increased continuously in worldwide, but no cure have been discovered. The etiology of IBD may include various factors such as genetics, epigenetic, environment as well as host immune system. Among the environmental factors of IBD, diet heavily influences gut health, especially non-digestible dietary fiber can have a great impact on selective growth of beneficial gut microbiota called probiotics. Seaweeds have been consumed in Asia countries and are a rich source for dietary fiber. Accumulated data have suggested the possibility of utilizing seaweed derived oligosaccharides as prebiotics to prevent IBD and its recurrence. In this review, seaweed derived oligosaccharides such as fucoidan and laminarin regarding gut health and potential therapeutic tools for IBD will be discussed based on studies conducted in vitro and in vivo models.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.sup2
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• pp.67-71
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• 2008

The incidence of inflammatory bowel disease (IBD), especially Crohn disease, in children is remarkably increasing in Korea. Therefore, it is necessary for pediatrician to be aware of the initial presentation of Crohn disease and ulcerative colitis. Laboratory tests, radiologic studies, and endoscopic procedures are helpful in differentiating between them. At the time of presentation, most of children with IBD have abdominal pain, diarrhea, hematochezia and/or weight loss. However, atypical presentation of these diseases may contribute to a delay in diagnosis.

• Journal of Life Science
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• v.23 no.3
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• pp.448-461
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• 2013

Inflammatory bowel disease, known as Crohn's disease and ulcerative colitis, is an unexplained disease characterized by chronic inflammation that repeats a cycle of relapse, improvement, and complications. The cause of inflammatory bowel disease is not clearly known, but it is predicted that a complex of various factors precipitate its occurrence. In particular, inflammatory mediators, such as cytokine, induce an increase in cell-mediated inflammatory responses. Focal tissue damage then occurs in the intestinal mucosa because of the weakening of the immune-modulating functions of cotton. Immune and inflammatory responses do not decrease appropriately but continue until they lead to chronic inflammation. Current research has focused on the cytokine genes, which have important roles in these inflammatory responses. Cytokine is a glycoprotein that is produced mostly in activated immune cells. It connects the activation, multiplication, and differentiation between immune cells, which causes focal tissue damage and inflammatory response. Moreover, butyrate, which originates in dietary fiber and plays an important role in the structure and function of the intestinal area, shows control functions in the intestinal immune system by decreasing the proinflammatory cytokine and increasing the anti-inflammatory cytokine. Therefore, this research investigated the molecular mechanism of the anti-inflammatory effects of butyrate to comprehend the cytokine controlling abilities of butyrate in the immune cells. Butyrate is expected to have potential in new treatment strategies for inflammatory bowel disease.

• Korean Journal of Clinical Laboratory Science
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• v.50 no.1
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• pp.11-19
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• 2018

The gut microbiome has been studied extensively over the past decade with most scientific reports focused on the adverse role of the gut microbiome on gastrointestinal diseases. For example, the altered gut microbiome exacerbates the development of immune system-mediated damage in many diseases. The most studied pathologies include irritable bowel syndrome, inflammatory bowel diseases, and colitis-associated cancer. On the other hand, intestinal microflora is also beneficial and contributes to the intestinal physiology by the synthesis of vitamins, production of short chain fatty acids and bile acid metabolism, thereby maintaining gut homeostasis. Therefore, the balance between commensal and pathogenic bacteria populations influences mainly the maintenance of intestinal health. Changes in the intestinal microflora have been suspected to be the underlying causes of multiple diseases. Despite the immense amount of published data, the optimal gut microbiome composition is still controversial. This review briefly outlines the connection between the gut microbiome and critical gastrointestinal diseases focusing on three prominent intestinal disorders: irritable bowel syndrome, inflammatory bowel diseases, and colitis-associated cancer disorders. Finally, intervention strategies using natural products for the alleviation of these diseases and the maintenance of a health gut microbiome are suggested.

• 한국유가공학회:학술대회논문집
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• 2007.09a
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• pp.49-58
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• 2007

Inflammatory process leads to the well-known mucosal damage and therefore a further disturbance of the epithelial barrier function, resulting abnormal intestinal wall function, even further accelerating the inflammatory process[1]. Despite of the records, etiology and pathogenesis of IBD remain rather unclear. There are many studies over the past couple of years have led to great advanced in understanding the inflammatory bowel disease(IBD) and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses including increased serum concentrations of different cytokines. Therefore, targeted molecules can be specifically eliminated in their expression directly on the transcriptional level. Interesting therapeutic trials are expected against adhesion molecules and pro-inflammatory cytokines such as TNF-${\alpha}$. The future development of immune therapies in IBD therefore holds great promises for better treatment modalities of IBD but will also open important new insights into a further understanding of inflammation pathophysiology. Treatment of cytokine inhibitors such as Immunex(Enbrel) and J&J/Centocor(Remicade) which are mouse-derived monoclonal antibodies have been shown in several studies to modulate the symptoms of patients, however, theses TNF inhibitors also have an adverse effect immune-related problems and also are costly and must be administered by injection. Because of the eventual development of unwanted side effects, these two products are used in only a select patient population. The present study was performed to elucidate the ability of TNF-${\alpha}$ antibodies produced in sheep colostrums to neutralize TNF-${\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. In vitro study, inhibitory effect of anti-TNF-${\alpha}$ antibody from the sheep was determined by cell bioassay. The antibody from the sheep at 1 in 10,000 dilution was able to completely inhibit TNF-${\alpha}$ activity in the cell bioassay. The antibodies from the same sheep, but different milkings, exhibited some variability in inhibition of TNF-${\alpha}$ activity, but were all greater than the control sample. In vivo study, the degree of inflammation was severe to experiment, despite of the initial pilot trial, main trial 1 was unable to figure out of any effect of antibody to reduce the impact of PAF and LPS. Main rat trial 2 resulted no significant symptoms like characteristic acute diarrhea and weight loss of colitis. This study suggested that colostrums from sheep immunized against TNF-${\alpha}$ significantly inhibited TNF-${\alpha}$ bioactivity in the cell based assay. And the higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent TNF-${\alpha}$ induced intestinal damage in the intact animal. Further study will require to find out an alternative animal model, which is more acceptable to test anti-TNF-${\alpha}$ IgA therapy for reducing the impact of inflammation on gut dysfunction. And subsequent pre-clinical and clinical testing also need generation of more antibody as current supplies are low.

• Food Industry And Nutrition
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• v.7 no.1
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• pp.50-54
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• 2002

• Clinical and Experimental Pediatrics
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• v.52 no.4
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• pp.504-507
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• 2009

Autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), and primary biliary cirrhosis (PBC) are chronic autoimmune liver diseases. Overlap syndrome is defined as a condition in which the clinical, biochemical, and histological features of these autoimmune diseases are overlapped. Thus, it is difficult to appreciate overlap syndrome as an actual diagnostic entity. Only a few cases of the overlap syndrome of AIH and PSC have been reported, especially in children. Moreover, PSC is known to be the most frequent liver disorder associated with inflammatory bowel diseases such as ulcerative colitis. We report one case of AIH-PSC overlap syndrome in a child who was diagnosed as having ulcerative colitis.

• Pediatric Infection and Vaccine
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• v.28 no.2
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• pp.110-117
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• 2021

Toxic megacolon is a fatal complication of inflammatory or infectious bowel disease. Prognosis depends on the severity of the disease. In cases of poor prognosis, clinical outcomes range from intestinal resection to death, so early diagnosis and appropriate treatment are very important. However, the prevalence of toxic megacolon in children is very low, and in those without underlying diseases such as inflammatory bowel disease, early diagnosis may be delayed. A previously healthy 12-year-old boy presented to our hospital with lower abdomen pain, fever, and hematochezia. Despite antibiotic therapy, the symptoms worsened. On the third day, abdominal computed tomography revealed severe dilatation of the transverse colon, which indicated toxic megacolon. Stool culture was positive for Salmonella enteritidis group D, and rectal endoscopy showed no signs of inflammatory bowel disease. Ceftriaxone and intravenous methylprednisolone were administered, and the patient's condition improved without any complications. We report a case of toxic megacolon as a complication of infectious colitis caused by S. enteritidis group D, which was diagnosed using early imaging and successfully treated without surgical intervention.

• Journal of Life Science
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• v.34 no.2
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• pp.138-144
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• 2024

Crocin is a major carotenoid of the Gardenia jasminoides fruit and Crocus sativus stigma (saffron), which are used in various cuisines as flavoring and coloring agents, as well as in phytomedicine for the treatment of several disorders, including headache, fever, edema, fatty liver, viral hepatitis, respiratory disease, menstruation disorders, insomnia, and hypertension. Crocin (C₄₄H₆₄O₂₄) is a chemical diester composed of the dicarboxylic acid crocetin and disaccharide gentiobiose. Many in vitro and in vivo studies have been conducted about the biological and pharmacological function and toxicity of crocin. Crocin has been revealed to have no genotoxicity and pathological manifestation. Crocin acts as an antioxidant, anti-cancer, memory enhancer, anxiolytic, antidepressant, aphrodisiac, anti-atherosclerotic, cardioprotector, and hepatoprotector. Here, an inclusive review of crocin is introduced based on previously explored studies referred to in the literature. Different studies have confirmed the protective role of crocin in the pathogenesis of inflammatory diseases, including inflammatory bowel diseases, gastritis, asthma, atherosclerosis, rheumatoid arthritis, multiple sclerosis, type 1 diabetes, Alzheimer's disease, Parkinson's disease, and depression. It is surmised that crocin suppresses inflammatory, antioxidant, and apoptotic processes through multiple mechanisms. Crocin is considered a safe and effective therapeutic choice for patients with inflammatory conditions, although more research investigating its mechanisms and results acquired in clinical trials are needed.

• Journal of Life Science
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• v.24 no.12
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• pp.1339-1344
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• 2014

Inflammatory bowel disease is an immune disorder associated with chronic mucosal inflammation and severe ulceration in the gastrointestinal tract. Antibodies against proinflammatory cytokines, including TNF${\alpha}$, are currently used as promising therapeutic agents against the disease. Stabilization of the transcript is a crucial post-transcriptional process in the expression of proinflammatory cytokines. In the present study, we assessed the expression and histological distribution of the HuR protein, an important transcript stabilizer, in tissues from experimental animals and patients with Crohn's disease. The total and cytosolic levels of the HuR protein were enhanced in the intestinal epithelia from dextran sodium sulfate (DSS)-treated mice compared to those in control tissues from normal mice. Moreover, the expression of HuR was very high only in the mucosal and glandular epithelium, and the relative localization of the protein was sequestered in the lower parts of the villus during the DSS insult. The expression of HuR was significantly higher in mucosal lesions than in normal-looking areas. Consistent with the data from the animal model, the expression of HuR was confined to the mucosal and glandular epithelium. These results suggest that HuR may contribute to the post-transcriptional regulation of proinflammatory genes during early mucosal insults. More mechanistic investigations are warranted to determine the potential use of HuR as a predictive biomarker or a promising target against IBD.