https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/607 2026-04-04T15:23:03Z 2026-04-04T15:23:03Z Baek, Hyun woo Park, Saemi Kim, Yeonhwa Hyun, Kyungtae Hong, Sumin Han, Eunjung Lee, Yunkyoung Kim, Hwee-Jin Rah, Yoon Chan Kim, Suhyun Choi, June https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/79049 2026-01-26T08:34:51Z 2025-12-01T00:00:00Z

Title: Comprehensive Evaluation of the Embryotoxicity and Ototoxicity of a Car Diffuser on Zebrafish Larvae: Impacts on Morphology and Hair Cells Authors: Baek, Hyun woo; Park, Saemi; Kim, Yeonhwa; Hyun, Kyungtae; Hong, Sumin; Han, Eunjung; Lee, Yunkyoung; Kim, Hwee-Jin; Rah, Yoon Chan; Kim, Suhyun; Choi, June Abstract: Diffusers release various chemical compounds into the environment, some of which may have ototoxic effects. Despite their widespread use, the safety profiles of these compounds remain largely unexplored. This study evaluated the potential toxicity of a car diffuser extract, Diff3, on zebrafish larvae by assessing morphology, survival rate, hair cell integrity, and rheotactic behavior. Forty wild-type zebrafish larvae at 4 h post-fertilization (hpf) were exposed to Diff3 and observed at 3 and 5 days post-fertilization (dpf) using a stereomicroscope. Hair cell damage was assessed using YO-PRO-1 iodide staining in four neuromasts and oxidative stress was measured in transgenic (Brn3C:EGFP) larvae using CellROX Deep Red Reagent. Rheotactic behavior was analyzed using a specialized behavioral testing system. No significant morphological changes or survival differences were observed between groups. However, hair cell counts were significantly reduced in Diff3-treated larvae, and ROS levels were notably higher in the treatment group. However, in additional experiments, no significant changes in rheotactic behavior were observed. These findings suggest that Diff3 induces hair cell loss through oxidative stress, which may affect sensory function. This study highlights the need to evaluate the ototoxic potential of household chemical products and emphasizes the importance of regulatory measures to ensure consumer safety. Further research is required to determine long-term effects and potential recovery mechanisms following exposure to such compounds.

2025-12-01T00:00:00Z Hyun, Kyungtae Lee, Yunkyoung Hong, Sumin Han, Eunjung Park, Saemi Baek, Hyun woo Kim, Hwee-Jin Rah, Yoon Chan Choi, June https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/78348 2025-11-13T00:31:08Z 2025-09-01T00:00:00Z

Title: In vivo and in vitro evaluation of the protective effects of osthole against ototoxicity using the zebrafish model and HEI-OC1 cell line Authors: Hyun, Kyungtae; Lee, Yunkyoung; Hong, Sumin; Han, Eunjung; Park, Saemi; Baek, Hyun woo; Kim, Hwee-Jin; Rah, Yoon Chan; Choi, June Abstract: Osthole, a coumarin derivative with potent antioxidant and anti-inflammatory properties, has demonstrated promising therapeutic potential in protecting against ototoxicity. This study investigated the protective effects of osthole through both in vitro and in vivo experimental models. A high-content screening of 1505 natural compounds in HEI-OC1 cells identified osthole as the most effective compound in alleviating gentamicin-induced cellular damage. Our results indicate that osthole confers protection by restoring autophagic flux and reducing the accumulation of reactive oxygen species (ROS). In HEI-OC1 cells, cell viability was significantly improved following co-treatment with gentamicin and osthole. Western blot analysis revealed that osthole modulates key signaling pathways involved in cell survival and autophagy. Furthermore, LysoTracker staining in zebrafish larvae confirmed that osthole preserved autophagic activity compromised by gentamicin exposure. In vivo experiments using wild-type and Tg(Brn3c:EGFP) zebrafish lines assessed neuromast hair cell survival in the lateral line system. Compared with the gentamicin-only group, the osthole co-treated group exhibited increased hair cell counts, a reduced number of TUNEL-positive apoptotic cells, decreased ROS levels, and enhanced autophagy. These outcomes collectively demonstrate the potential protective effects of osthole against gentamicin-induced ototoxicity in both cellular and zebrafish models. Taken together, these findings highlight osthole as a promising candidate for therapeutic development against aminoglycoside-induced hearing loss, offering a multi-targeted mechanism involving oxidative stress reduction, autophagy restoration, and inhibition of apoptosis.

2025-09-01T00:00:00Z Lee, Hong Kim, Yeonhwa Cho, Yuji Jeon, Eun Jung Jeong, Sang Hoon Lee, Ju-Han Kim, Suhyun https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/77082 2025-11-12T06:02:10Z 2025-08-01T00:00:00Z

Title: Nociceptive effects and gene alterations of CMIT/MIT mixture in zebrafish embryos and larvae Authors: Lee, Hong; Kim, Yeonhwa; Cho, Yuji; Jeon, Eun Jung; Jeong, Sang Hoon; Lee, Ju-Han; Kim, Suhyun Abstract: Nociception is a critical biological process that facilitates detecting and avoiding harmful stimuli. Methylisothiazolinone (MIT) and methylchloroisothiazolinone (CMIT) are biocidal agents widely used in disinfectants and cosmetics, however, their effects on nociceptive pathways and neurotoxicity remain insufficiently understood. This study investigated the neurotoxic and nociceptive effects of CMIT/MIT mixtures in zebrafish models. Zebrafish embryos were exposed to CMIT/MIT, and their behavioral and molecular responses to nociceptive stimuli were assessed. Acute exposure (4 −72 h post-fertilization) to CMIT/MIT (15 and 30 μg/L) led to heightened behavioral responses to noxious stimuli, significantly increasing velocity and neuronal activity. Molecular analysis revealed the upregulated expression of nociception-related and inflammatory markers. Subchronic exposure (4 hpf to 28 days post-fertilization) to lower CMIT/MIT concentrations resulted in prolonged freezing responses and reduced the movement in zebrafish larvae. Protein-protein interaction analysis further identified key pathways, including calcium signaling, MAPK, and neuroinflammation, affected by CMIT/MIT exposure. This study provides evidence that even low levels of CMIT/MIT exposure can enhance nociceptive responses by activating sensory neurons and modulating inflammatory pathways, raising concerns about the neurotoxic potential of these widely used biocidal compounds. © 2025 Elsevier B.V.

2025-08-01T00:00:00Z Lee, Yunkyoung Jung, Inyoung Lee, Dong-Won Seo, Yongbo Kim, Suhyun Park, Hae-Chul https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/77109 2025-07-10T02:11:43Z 2025-06-01T00:00:00Z

Title: Transforming growth factor-β receptor I kinase plays a crucial role in oligodendrocyte regeneration after demyelination Authors: Lee, Yunkyoung; Jung, Inyoung; Lee, Dong-Won; Seo, Yongbo; Kim, Suhyun; Park, Hae-Chul Abstract: Multiple sclerosis (MS) is an autoimmune disease characterized by the loss of oligodendrocytes (OLs) and axon demyelination in the central nervous system. Most therapeutic agents focus on regulating the immune response by suppressing autoimmune reactions. Therefore, developing therapeutic agents that promote remyelination by OLs at disease sites that have already undergone demyelination is necessary. In this study, we generated a new transgenic zebrafish with high efficiency for OL ablation and established a high-throughput screening (HTS)-based platform to identify therapeutic candidates that promote remyelination. Next, we screened a library of kinase inhibitors and identified one candidate, a transforming growth factor-β receptor I (TGF-βRI) kinase inhibitor. Treatment with this kinase inhibitor rapidly recruited microglia to induce clearance of myelin debris, early after OL removal. It also increased the proliferation of OL progenitor cells in demyelinating zebrafish larvae, resulting in restored OL numbers and reduced locomotor activity. Based on these results, we expect our HTS-based platform, along with our newly developed zebrafish model, to be very useful for identifying therapeutic agents that promote remyelination. Furthermore, since the candidate TGF-βRI kinase inhibitor identified in this study restored the phenotype following demyelination, we suggest that TGF-βRI kinase may potentially be a therapeutic target for the treatment of demyelinating diseases. © 2025 The Authors

2025-06-01T00:00:00Z