Apelin protects auditory cells from cisplatin-induced toxicity in vitro by inhibiting ROS and apoptosis

Area of Science:

• Ototoxicity research
• Cellular and Molecular Biology
• Pharmacology

Background:

• Cisplatin is an effective anticancer drug but causes ototoxicity, damaging cochlear hair cells.
• Apelin, an endogenous peptide, is known to counteract oxidative stress and apoptosis.
• The protective role of Apelin against cisplatin-induced ototoxicity remains to be fully elucidated.

Purpose of the Study:

• To investigate the protective effects of Apelin against cisplatin-induced ototoxicity in vitro.
• To explore the underlying mechanisms of Apelin's protective action.

Main Methods:

• Utilized the mouse auditory cell line HEI-OC1 and cochlear explants.
• Administered cisplatin and exogenous Apelin to assess cellular responses.
• Measured apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential, JNK signaling pathway activation, and pro-apoptotic factor expression.

Main Results:

• Apelin is expressed in HEI-OC1 cells and cochlear hair cells (HCs) and is downregulated by cisplatin.
• Pre-treatment with Apelin significantly reduced cisplatin-induced apoptosis and injury in HEI-OC1 cells and HCs.
• Apelin attenuated ROS generation, preserved mitochondrial membrane potential, inhibited JNK signaling, and decreased pro-apoptotic factors.

Conclusions:

• Apelin demonstrates significant otoprotective effects against cisplatin-induced toxicity.
• Apelin mitigates cisplatin-induced ototoxicity by reducing oxidative stress, apoptosis, and JNK pathway activation.
• Apelin holds potential as an otoprotective agent for preventing cisplatin-induced hearing loss.