Kyung Hee University · Medicine
Professor Hyeung-Jin Jang's research lab focuses on molecular mechanisms underlying metabolic and inflammatory diseases, with a central emphasis on gut-brain axis signaling, incretin hormone regulation, and targeted cancer therapeutics. The lab investigates the role of taste receptors in enteroendocrine L-cells to understand how dietary nutrients like glucose stimulate GLP-1 secretion, offering insights into novel, safer alternatives to GLP-1 mimetic drugs. Additionally, the lab develops advanced nanotherapeutics—particularly biodegradable porous silicon nanoparticles—for targeted delivery of anti-miRNA agents in ovarian cancer and explores natural compounds like ginsenosides for their anti-inflammatory effects in lung and epithelial tissues via NF-κB modulation.
Figures are computed from collected data and may differ slightly.
Glucagon-like peptide-1 (GLP-1), released from gut endocrine L cells in response to glucose, regulates appetite, insulin secretion, and gut motility. How glucose given orally, but not systemically, induces GLP-1 secretion is unknown. We show that human duodenal L cells express sweet taste receptors, the taste G protein gustducin, and several other taste transduction elements. Mouse intestinal L cells also express alpha-gustducin. Ingestion of glucose by alpha-gustducin null mice revealed deficie
Silencing of aberrantly expressed microRNAs (miRNAs or miRs) has emerged as one of the strategies for molecular targeted cancer therapeutics. In particular, miR-21 is an oncogenic miRNA overexpressed in many tumors, including ovarian cancer. To achieve efficient administration of anti-miR therapeutics, delivery systems are needed that can ensure local accumulation in the tumor environment, low systemic toxicity, and reduced adverse side effects. In order to develop an improved anti-miR therapeut
Taste receptors exist in several organs from tongue to colon and have diverse functions dependent on specific cell type. In enteroendocrine L-cells, stimulation of taste receptor signaling induces incretin hormones. Among incretin hormones, glucagon-like peptide-1 (GLP-1) induces insulinotropic action by activating GLP-1 receptor of pancreatic β-cells. However, GLP-1 mimetic medicines have reported clinical side effects, such as autoimmune hepatitis, acute kidney injury, pancreatitis, and pancre
<i>Objective</i>. There is limited information of the anti-inflammatory effects of Rg3 on inflamed lung cells and tissues. Therefore, we confirmed the anti-inflammatory mechanism of ginsenoside Rg3 in inflamed human airway epithelial cells (A549) and tissues whether Rg3 regulates nuclear factor kappa B (NF-<i>κ</i>B) activity. <i>Methods</i>. To induce the inflammation, IL-1<i>β</i> (10 ng/ml) was treated to A549 cells for 4 h. The effects of Rg3 on NF-<i>κ</i>B activity and COX-2 expression wer
By using microarray analysis that enables us to simultaneously and globally examine the complete transcriptome during cellular responses, we have revealed novel information regarding the mode of action of OPP on Staphylococcus: OPP inhibits anabolism of many amino acids and highly downregulates the genes that encode the enzymes involved in the DAP pathway. Lysine and DAP are essential for building up the peptidoglycan cell wall. It was concluded that the mode of action of OPP is similar to the m
The results of this study suggest that Emb may be used as an anti-inflammatory agent via inhibition of NF-κB and related cytokines.
Obesity is a risk factor for metabolic diseases including type 2 diabetes, nonalcoholic steatohepatitis (NASH), heart diseases, and cancer. This study aimed to investigate the anti-obesity effect of Polygalin C (PC) isolated from <i>Polygala japonica</i> Houtt. in 3T3-L1 adipocytes. Based on Oil Red O assay results, PC significantly decreased lipid accumulation compared to the control. We found that PC suppressed adipogenesis transcription factors including peroxisome proliferator-activated rece
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