International journal of pediatric otorhinolaryngology · 2025
Therapeutic potential of intraperitoneal emodin on cisplatin ototoxicity in rats.
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Ozdemir Ozan, Keskin Ezgi, Esrefoglu Mukaddes, Guler Eray Metin, Hekimoglu Emine Rumeysa, Akdemir Enise, Bozalı Kubra, Yigit Ozgur
Аннотация
OBJECTIVES: Cisplatin is an effective chemotherapeutic agent used in the treatment of various types of cancer; however, it exhibits severe ototoxic side effects. The aim of this study is to investigate the potential protective effects of emodin, a natural anthraquinone derivative, against cisplatin-induced ototoxicity in a rat model.
METHODS: Twenty-four female Wistar rats were divided into four groups: control, emodin, cisplatin, and emodin + cisplatin. Auditory brainstem responses (ABR) were measured on days 1, 3, and 7 using click and tone burst stimuli (8-32 kHz). Following sacrifice, cochlear tissues were evaluated through histological and biochemical analyses. For biochemical assessment, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were measured. Histological changes were examined using light microscopy.
RESULTS: A significant increase in hearing thresholds, severe damage to the histological structure of the cochlea, and elevated total oxidant levels were observed in the cisplatin group (p < 0.05). In the emodin + cisplatin group, compared to the cisplatin group, the increase in hearing thresholds and histological damage were found to be less pronounced (p < 0.05). Furthermore, the increase in total antioxidant levels and the decrease in oxidative stress index support the protective effect of emodin against oxidative stress (p < 0.05).
CONCLUSION: Emodin has demonstrated protective effects against cisplatin-induced ototoxicity. These findings highlight the potential of emodin as an otoprotective agent and support its possible application during cisplatin therapy. However, further research is required for clinical implementation.
METHODS: Twenty-four female Wistar rats were divided into four groups: control, emodin, cisplatin, and emodin + cisplatin. Auditory brainstem responses (ABR) were measured on days 1, 3, and 7 using click and tone burst stimuli (8-32 kHz). Following sacrifice, cochlear tissues were evaluated through histological and biochemical analyses. For biochemical assessment, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were measured. Histological changes were examined using light microscopy.
RESULTS: A significant increase in hearing thresholds, severe damage to the histological structure of the cochlea, and elevated total oxidant levels were observed in the cisplatin group (p < 0.05). In the emodin + cisplatin group, compared to the cisplatin group, the increase in hearing thresholds and histological damage were found to be less pronounced (p < 0.05). Furthermore, the increase in total antioxidant levels and the decrease in oxidative stress index support the protective effect of emodin against oxidative stress (p < 0.05).
CONCLUSION: Emodin has demonstrated protective effects against cisplatin-induced ototoxicity. These findings highlight the potential of emodin as an otoprotective agent and support its possible application during cisplatin therapy. However, further research is required for clinical implementation.