Seoul National University · Medicine
Professor Joo Sung Kim's research lab focuses on gastrointestinal inflammation, infectious diseases, and the molecular mechanisms underlying inflammatory bowel disease (IBD) and Helicobacter pylori-related disorders. The lab investigates key signaling pathways such as NF-κB and cytokine regulation in intestinal epithelial cells, exploring how natural compounds like luteolin and drugs like metformin modulate these pathways to exert anti-inflammatory and anti-tumorigenic effects. A major emphasis is placed on understanding the interplay between host immunity, chronic inflammation, and cancer development in the gastrointestinal tract, particularly in colorectal and gastric cancers. The lab also examines epidemiological and genetic factors, including cytokine polymorphisms and H. pylori seroprevalence, to identify risk markers and therapeutic targets.
Figures are computed from collected data and may differ slightly.
These results indicate that metformin suppresses NF-κB activation in intestinal epithelial cells and ameliorates murine colitis and colitis-associated tumorigenesis in mice, suggesting that metformin could be a potential therapeutic agent for the treatment of inflammatory bowel disease.
The nuclear factor (NF)-kappaB transcriptional system is a major effector pathway involved in inflammation and innate immune responses. The flavonoid luteolin is found in various herbal extracts and has shown anti-inflammatory properties. However, the mechanism of action and impact of luteolin on innate immunity is still unknown. We report that luteolin significantly blocks lipopolysaccharide (LPS)-induced IkappaB phosphorylation/degradation, NF-kappaB transcriptional activity and intercellular
Visceral obesity was found to be an independent risk factor of colorectal adenoma, and insulin resistance was associated with the presence of colorectal adenoma.
To identify the risk of gastric cancer in first-degree relatives of gastric cancer patients, and to determine if there is an interaction between Helicobacter pylori (H. pylori) infection and family history of gastric cancer in gastric carcinogenesis.It is unclear to what degree a family history of gastric cancer is associated with stomach cancer risk in Korea.From May 2003 to July 2008, 428 gastric cancer patients and 368 controls were included in the analyses. Logistic regression models includi
These results suggest that the genetic polymorphisms of these 3 inflammation-related cytokines, IL-10, IL-8, and IL-6, are associated with the development of H. pylori-associated gastroduodenal disease.
The aims of this study were to demonstrate the trends in seropositivity and the eradication therapy rate for Helicobacter pylori (H. pylori) over an 18-year period in an asymptomatic Korean population and to explore the factors associated with H. pylori seropositivity and its eradication therapy. In total, 23,770 subjects (aged 17-97 years) from a health examination center participated in this cross-sectional study from January 2016 to June 2017. Questionnaires that included questions about the
The aim of this study was to demonstrate the anti-inflammatory effect of <i>Lactobacillus kefirgranum</i> PRCC-1301-derived extracellular vesicles (PRCC-1301 EVs) on intestinal inflammation and intestinal barrier function. Human intestinal epithelial cells (IECs) Caco-2 were treated with PRCC-1301 EVs and then stimulated with dextran sulfate sodium (DSS). Real-time RT-PCR revealed that PRCC-1301 EVs inhibited the expression of pro-inflammatory cytokines in Caco-2 cells. PRCC-1301 EVs enhanced in
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