https://scholar.dgist.ac.kr/handle/20.500.11750/890 2026-10-27T07:55:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/61002 Title: Inotodiol prevents age-related muscle wasting by restoring mitochondrial function through liver X receptor beta signaling Author(s): You, Chang-Lim; Bae, Ju-Hyeon; Jeong, Yideul; Leem, Young-Eun; Kim, June; Park, Jeongmin; Vuong, Tuan Anh; Jang, Jiwoong; Park, Sanghee; Lee, Young-Sam; Ji, Moongi; Paik, Man-Jeong; Kim, IL-Young; Lee, Sang-Jin; Bae, Gyu-Un; Kang, Jong-Sun Abstract: Sarcopenia is characterized by a progressive decline in muscle mass and strength and represents a major contributor to increased mortality in the elderly population. Mitochondrial dysfunction, which leads to impaired energy metabolism and elevated oxidative stress, is a key driver of muscle wasting and associated metabolic disorders. Thus, mitochondrial targeting is a promising strategy for combating sarcopenia. In this study, we investigated the therapeutic potential of the mycosterol inotodiol (Ino) in mitigating age-related muscle wasting and metabolic dysfunction. Ino treatment significantly improved muscle mass and function in aged mice and prevented dexamethasone (DEX)-induced muscle atrophy. Ino enhanced mitochondrial function and restored muscle metabolism, as evidenced by increased mitochondrial content, elevated oxidative capacity, reduced lipid accumulation, and decreased oxidative stress. In addition, Ino attenuated palmitic acid (PA)-induced lipotoxicity in muscle cells by restoring lipid metabolism. Further investigation revealed that Ino activates liver X receptor beta (LXR beta) and promotes its interaction with peroxisome proliferator-activated receptor delta (PPAR delta), thereby increasing sirtuin 3 (Sirt3) transcription. Consequently, Ino activates the LXR beta/SIRT3/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) signaling pathway, a central regulator of mitochondrial function and metabolic homeostasis. Collectively, these findings identify Ino as a promising therapeutic candidate for preserving mitochondrial function and alleviating age-associated muscle dysfunction. 2026-08-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60356 Title: SLIT2 as a key regulator and therapeutic target in liver injury Author(s): Choi, Yongwon; Choi, Jae-ho; Lee, Young-Sam; Jeong, Jinju; Kang, Eunho; Park, So-hyun; Lee, Young-kyoung; Park, Soon-sang; Kang, Hee-young; Kim, Young-hwa; Park, Tae-jun Abstract: Drug-induced liver injury accounts for approximately 10% of acute hepatitis and up to 50% of acute liver failure. Despite its clinical significance, treatment remains largely limited to cessation of the offending agent. SLIT/ROBO signaling, known for roles in organ development, angiogenesis, leukocyte migration, and cancer metastasis, has demonstrated protective effects against various organ damage. In mouse models of liver injury induced by acetaminophen (APAP), thioacetamide, bile duct ligation, and serum from patients with toxic liver disease, Slit2 expression significantly increases, while Slit1 and Slit3 remain unchanged. Liver-specific Slit2 knockdown exacerbates liver injury, whereas recombinant SLIT2 alleviates liver damage by reducing oxidative stress via CYP2E1 downregulation and suppressing inflammation through nuclear factor κB inhibition. Notably, among ROBO receptors, only ROBO4 was induced in hepatocytes after APAP exposure. ROBO4 knockdown eliminates the hepatoprotective effects of SLIT2, highlighting the importance of SLIT2/BOBO4 signaling in toxic liver injury. Furthermore, the novel Slit2-derived peptide 5 (SP5), designed from the ROBO4-binding LRR2 domain, significantly reduces liver damage and inflammation. Notably, both recombinant SLIT2 and SP5 confer hepatoprotection even when administered 24 h after APAP challenge. These findings suggest that SLIT2/ROBO4-targeted therapies may offer a promising approach for preventing fulminant hepatitis in the context of toxic liver injury. 2026-03-31T15:00:00Z 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. 2025-12-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/57310 Title: Brief guide to senescence assays using cultured mammalian cells Author(s): Kang, Eunseok; Kang, Chanhee; Lee, Young-Sam; Lee, Seung-Jae V. Abstract: Cellular senescence is a crucial biological process associated with organismal aging and many chronic diseases. Here, we present a brief guide to mammalian senescence assays, including the measurement of cell cycle arrest, change in cellular morphology, senescence-associated β-galactosidase (SA-β-gal) staining, and the expression of senescence-associated secretory phenotype (SASP). This work will be useful for biologists with minimum expertise in cellular senescence assays. © 2024 The Author(s) 2024-08-31T15:00:00Z