Cisplatin is a widely used platinum-based chemotherapeutic agent that often causes irreversible hair cell loss, leading to hearing impairment. To date, effective strategies for preventing cisplatin-induced ototoxicity remain limited. Corchorus olitorius L. (COL) is rich in bioactive phytochemicals with antioxidant and anti-inflammatory properties; however, the protective role of COL stem against cisplatin-induced hearing loss has not been explored. This study aimed to determine whether COL stem extract treatment could mitigate cisplatin-induced hair cell damage in the lateral line system of zebrafish. Herein, we use 7-day post-fertilization (dpf) transgenic zebrafish larvae as a high-throughput screening platform to assessed COL stem extract against cisplatin-induced hair cell injury. Endpoints included mechanotransduction (MET) function, reactive oxygen species (ROS) production, apoptotic and inflammatory responses, and locomotor behavior. Antioxidant capacity and acute toxicity were also evaluated. Pretreatment with COL stem extract preserved hair cell viability, restored MET function, reduced ROS accumulation, upregulated Nrf-2-dependent cytoprotective genes, suppressed apoptosis, and attenuated macrophage infiltration. The recovery of swimming behavior correlated with hair cell protection, confirming the phenotypic relevance. This study demonstrates, for the first time, that COL stem exerts potent otoprotective effects through antioxidative, anti-apoptotic, and anti-inflammatory mechanisms, contributes to maintain mechanosensory function and swimming behavior. The findings support COL stem as a promising candidate for otoprotection and validate zebrafish-based high-throughput screening for novel therapeutic discovery.

Adverse effects associated with prolonged corticosteroid therapy are strongly associated with increased intraocular pressure (IOP), which may progress to iatrogenic glaucoma and irreversible blindness if left untreated. Developing reliable animal models is essential for investigating corticosteroid-induced ocular hypertension and evaluating potential therapeutic strategies. In this study, we established a simple and non-invasive rat model of corticosteroid-induced ocular hypertension using topical application of Rinderon-A ointment. Longitudinal IOP measurements were performed weekly using a Tono-Pen in conscious rats throughout the 11-week experimental period. Rinderon-A treatment resulted in sustained bilateral IOP elevation, with an initial increase observed at week 1 (28.4 ± 1.5 mmHg) and a maximal mean IOP of 31.2 ± 0.7 mmHg at week 10. Rinderon-A-treated eyes exhibited a sustained ocular hypertensive response throughout the experimental period. Collectively, this model provides a reproducible platform for studying corticosteroid-associated ocular hypertension and may facilitate future investigations of therapeutic interventions.