Tekin Mustafa Said, Ayçiçek Abdullah, Bucak Abdulkadir, Ulu Şahin, Okur Erdoğan
Otolaryngology - Head and Neck Surgery, Medipol University Medipol Mega Hospital, Istanbul, TUR.
Otolaryngology - Head and Neck Surgery, Afyonkarahisar Health Sciences University Hospital, Afyonkarahisar, TUR.
Cureus. 2024 Oct 23;16(10):e72181. doi: 10.7759/cureus.72181. eCollection 2024 Oct.
Background The aim of this study was to investigate the protective effect of thymoquinone, an antioxidant, on hearing loss induced by acoustic trauma in rats. Material and methods This study included 32 Wistar Albino rats divided into four groups: control, acoustic trauma, thymoquinone + acoustic trauma, and thymoquinone only, with eight rats per group. The control group received 0.5 mL of corn oil intraperitoneally for 10 days. The acoustic trauma group was exposed to 100 dB white noise at 4 kHz for 16 hours. The thymoquinone + acoustic trauma group received thymoquinone (10 mg/kg) intraperitoneally for two days before acoustic trauma and eight days after acoustic trauma. The thymoquinone only group received thymoquinone (10 mg/kg) for 10 days. Distortion product otoacoustic emissions (DPOAEs) were measured before and after treatments on days 1, 4, and 10. Results In the control group, DPOAE measurements showed no significant change over the study period. The acoustic trauma group exhibited a significant decrease in DPOAE on the first day after trauma, followed by some recovery. The thymoquinone + acoustic trauma group showed no significant decrease in DPOAE on the first day post-trauma, suggesting a protective effect. The thymoquinone only group also indicated no significant change in DPOAE measurements, suggesting that thymoquinone alone did not affect hearing function. Conclusion Thymoquinone demonstrated a protective effect against acoustic trauma-induced hearing loss in rats, as evidenced by stable DPOAE measurements post-trauma. These findings suggest that thymoquinone may help preserve hearing function by reducing oxidative stress in the cochlea. Further studies are needed to confirm these results in humans and optimize dosage and treatment protocols.
背景 本研究的目的是调查抗氧化剂百里醌对大鼠声创伤所致听力损失的保护作用。
材料与方法 本研究纳入32只Wistar白化大鼠,分为四组:对照组、声创伤组、百里醌+声创伤组和单纯百里醌组,每组8只大鼠。对照组腹腔注射0.5 mL玉米油,持续10天。声创伤组暴露于4 kHz的100 dB白噪声中16小时。百里醌+声创伤组在声创伤前2天及声创伤后8天腹腔注射百里醌(10 mg/kg)。单纯百里醌组接受百里醌(10 mg/kg)治疗10天。在第1、4和10天治疗前后测量畸变产物耳声发射(DPOAE)。
结果 在对照组中,DPOAE测量在研究期间无显著变化。声创伤组在创伤后第一天DPOAE显著下降,随后有所恢复。百里醌+声创伤组在创伤后第一天DPOAE无显著下降,表明有保护作用。单纯百里醌组DPOAE测量也无显著变化,表明单独使用百里醌不影响听力功能。
结论 百里醌对大鼠声创伤所致听力损失具有保护作用,创伤后DPOAE测量结果稳定证明了这一点。这些发现表明,百里醌可能通过降低耳蜗中的氧化应激来帮助维持听力功能。需要进一步研究在人类中证实这些结果并优化剂量和治疗方案。