https://scholar.dgist.ac.kr/handle/20.500.11750/11719 Wed, 08 Apr 2026 22:10:48 GMT 2026-04-08T22:10:48Z https://scholar.dgist.ac.kr/handle/20.500.11750/59989 Title: Hydrogen Evolution via Oxygen Tolerant [NiFe]-Hydrogenase Immobilized on TiO2 Nanotubes Author(s): Kim, Hwapyong; Kim, Ki Nam; Lee, Sang-Hyeon; Nam, Chang-Hoon; Lee, Young-Sam; In, Su-Il Abstract: [FeFe]-hydrogenase has been of great interest due to its high enzymatic activity for hydrogen evolution reactions (HERs). However, the big challenge of [FeFe]-hydrogenase is a significant performance degradation in aerobic conditions. On the other hand, [NiFe]-hydrogenase of E. coli has an oxygen tolerant property. Therefore, using [NiFe]-hydrogenase is an effective solution to avoid performance degradation in aerobic conditions. Herein, we extracted [NiFe]-hydrogenases from E. coli and immobilized them on the TiO2 nanotube (TNT) electrode prepared by pyrrole-based electropolymerization for application in aerobic conditions. As a result, we can confirm that [NiFe]-hydrogenases coated TNT electrode demonstrates the increased HER activity underaerobic condition than control samples in in-vitro activity test using methylene viologen and linear sweep voltammetry. Wed, 31 Dec 2025 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/59989 2025-12-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/59369 Title: Targeting PON2 with Vutiglabridin Restores Mitochondrial Integrity and Attenuates Oxidative Stress-Induced Senescence Author(s): Heo, Jin-Woong; Kim, Hyeong Hwan; Lee, Jae Ho; Lee, Hyeong Min; Park, Hyung Soon; Nam, Chang-Hoon Abstract: Oxidative stress-induced mitochondrial dysfunction has been identified as a central driver of cellular senescence and age-related degeneration. The present study investigated the potential of vutiglabridin, a paraoxonase 2 (PON2) agonist, to mitigate reactive oxygen species (ROS)-induced senescence in human LO2 hepatocytes. The process of senescence was induced by the administration of hydrogen peroxide, followed by the recovery of the cells in fresh medium. The levels of intracellular ROS, the senescence-associated β-galactosidase staining, the p16/p21 expression, and the mitochondrial morphology were the focus of a comprehensive assessment utilizing a range of analytical techniques, including microscopy, quantitative PCR, and Western blotting. The present study demonstrated that the administration of vutiglabridin resulted in a dose-dependent reduction in attenuation of the expression of senescence markers. Transmission electron microscopy (TEM) and stimulated emission depletion (STED) imaging revealed the preservation of mitochondrial structure and network connectivity in cells treated with vutiglabridin. These effects were absent in PON2 knockout cells, confirming that vutiglabridin’s action requires functional PON2. The present study demonstrates that vutiglabridin alleviates oxidative stress-induced cellular senescence by preserving mitochondrial integrity and redox balance via a PON2-dependent mechanism. This study lends further support to the investigation of the PON2 pathway as a therapeutic target in age-related cellular dysfunction. Fri, 31 Oct 2025 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/59369 2025-10-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/57266 Title: Insights into an indolicidin-derived low-toxic anti-microbial peptide's efficacy against bacterial cells while preserving eukaryotic cell viability Author(s): Kim, Jihyun; Lee, Jieun; Kang, Eunho; Lee, Kyoungmin; Lee, Kyungeun; Cheon, Yeongmi; Lee, Seongsoo; Kim, Bokyung; Ko, Young Ho; Kim, Jin Hae; In, Su Il; Nam, Chang-Hoon Abstract: Antimicrobial peptides (AMPs) are a current solution to combat antibiotic resistance, but they have limitations, including their expensive production process and the induction of cytotoxic effects. We have developed novel AMP candidate (peptide 3.1) based on indolicidin, among the shortest naturally occurring AMP. The antimicrobial activity of this peptide is demonstrated by the minimum inhibitory concentration, while the hemolysis tests and MTT assay indicate its low cytotoxicity. In optical diffraction tomography, red blood cells treated with peptide 3.1 showed no discernible effects, in contrast to indolicidin. However, peptide 3.1 did induce cell lysis in E. coli, leading to a reduced potential for the development of antibiotic resistance. To investigate the mechanism underlying membrane selectivity, the structure of peptide 3.1 was analyzed using nuclear magnetic resonance spectroscopy and molecular dynamics simulations. Peptide 3.1 is structured with an increased distinction between hydrophobic and charged residues and remained in close proximity to the eukaryotic membrane. On the other hand, peptide 3.1 exhibited a disordered conformation when approaching the prokaryotic membrane, similar to indolicidin, leading to its penetration into the membrane. Consequently, it appears that the amphipathicity and structural rigidity of peptide 3.1 contribute to its membrane selectivity. In conclusion, this study may lead to the development of Peptide 3.1, a promising commercial candidate based on its low cost to produce and low cytotoxicity. We have also shed light on the mechanism of action of AMP, which exhibits selective toxicity to bacteria while not damaging eukaryotic cells. © 2024 International Union of Biochemistry and Molecular Biology. Tue, 31 Dec 2024 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/57266 2024-12-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/47978 Title: Vutiglabridin Alleviates Cellular Senescence with Metabolic Regulation and Circadian Clock in Human Dermal Fibroblasts Author(s): Heo, Jin-Woong; Lee, Hye-Eun; Lee, Jimin; Choi, Leo Sungwong; Shin, Jaejin; Mun, Ji-Young; Park, Hyung-Soon; Park, Sang-Chul; Nam, Chang-Hoon Abstract: The process of cellular senescence, which is characterized by stable cell cycle arrest, is strongly associated with dysfunctional cellular metabolism and circadian rhythmicity, both of which are reported to result from and also be causal to cellular senescence. As a result, modifying any of them—senescence, metabolism, or the circadian clock—may affect all three simultaneously. Obesity accelerates aging by disrupting the homeostasis of reactive oxygen species (ROS) via an increased mitochondrial burden of fatty acid oxidation. As a result, if senescence, metabolism, and circadian rhythm are all linked, anti-obesity treatments may improve metabolic regulation while also alleviating senescence and circadian rhythm. Vutiglabridin is a small molecule in clinical trials that improves obesity by enhancing mitochondrial function. We found that chronic treatment of senescent primary human dermal fibroblasts (HDFs) with vutiglabridin alleviates all investigated markers of cellular senescence (SA-β-gal, CDKN1A, CDKN2A) and dysfunctional cellular circadian rhythm (BMAL1) while remarkably preventing the alterations of mitochondrial function and structure that occur during the process of cellular senescence. Our results demonstrate the significant senescence-alleviating effects of vutiglabridin, specifically with the restoration of cellular circadian rhythmicity and metabolic regulation. These data support the potential development of vutiglabridin against aging-associated diseases and corroborate the intricate link between cellular senescence, metabolism, and the circadian clock. © 2024 by the authors. Sun, 31 Dec 2023 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/47978 2023-12-31T15:00:00Z