Balloon Eustachian Tuboplasty Combined or Not with Myringotomy in Eustachian Tube Dysfunction.

BACKGROUND: Eustachian tube dysfunction (ETD) is a common disorder causing ear pressure, pain, and hearing loss. Balloon Eustachian tuboplasty (BET) is an emerging technique for dilating the Eustachian tube and treating ETD. Whether adding myringotomy improves BET efficacy is controversial. METHODS: This retrospective study included 95 ETD patients undergoing BET alone (n = 44) or BET with myringotomy (BET + M; n = 51) between June 2020 and August 2021 at a single medical center. The primary outcome was the change in ETDQ-7 symptom scores from baseline to 6 months after treatment. Secondary outcomes included audiometry, endoscopy, Valsalva maneuver, and complications. RESULTS: The ETDQ-7 scores improved significantly after treatment in both groups (p < 0.001), without significant between-group differences (p = 0.417). No significant differences occurred in the audiometry, endoscopy, and Valsalva results or in most complications between groups. One BET + M patient had a persistent tympanic membrane perforation. CONCLUSIONS: Both BET alone and BET + M effectively and safely improved the subjective and objective ETD outcomes. However, adding myringotomy did not further improve the outcomes over BET alone, while it incurred risks such as persistent perforation. BET alone may sufficiently treat ETD without requiring myringotomy in this cohort. Further randomized controlled trials should identify optimal candidates for BET alone versus combined approaches.

Otoprotective Effects of Fucoidan Reduce Cisplatin-Induced Ototoxicity in Mouse Cochlear UB/OC-2 Cells.

Cisplatin is a widely used standard chemotherapy for various cancers. However, cisplatin treatment is associated with severe ototoxicity. Fucoidan is a complex sulfated polysaccharide mainly derived from brown seaweeds, and it shows multiple bioactivities such as antimicrobial, anti-inflammatory, anticancer, and antioxidant activities. Despite evidence of the antioxidant effects of fucoidan, research on its otoprotective effects remains limited. Therefore, the present study investigated the otoprotective effects of fucoidan in vitro using the mouse cochlear cell line UB/OC-2 to develop new strategies to attenuate cisplatin-induced ototoxicity. We quantified the cell membrane potential and analyzed regulators and cascade proteins in the apoptotic pathway. Mouse cochlear UB/OC-2 cells were pre-treated with fucoidan before cisplatin exposure. The effects on cochlear hair cell viability, mitochondrial function, and apoptosis-related proteins were determined via flow cytometry, Western blot analysis, and fluorescence staining. Fucoidan treatment reduced cisplatin-induced intracellular reactive oxygen species production, stabilized mitochondrial membrane potential, inhibited mitochondrial dysfunction, and successfully protected hair cells from apoptosis. Furthermore, fucoidan exerted antioxidant effects against oxidative stress by regulating the Nrf2 pathway. Therefore, we suggest that fucoidan may represent a potential therapeutic agent for developing a new otoprotective strategy.

Bisdemethoxycurcumin-mediated Attenuation of Apoptosis Prevents Gentamicin-induced Ototoxicity in Mouse Cochlear UB/OC-2 Cells.

BACKGROUND/AIM: Gentamicin has been widely prescribed since the last two decades despite its ototoxicity and nephrotoxicity. Bisdemethoxycurcumin (BDMC) is an affordable and safe curcuminoid with medicinal properties. We aimed to understand the effects of BDMC on the gentamicin-induced hair cell damage in mouse cochlear UB/OC-2 cells, in order to elucidate the therapeutic potential of BDMC against gentamicin-induced ototoxicity. MATERIALS AND METHODS: We quantified the cell membrane potential and examined the regulators and cascade proteins in the intrinsic pathway of hair cell apoptosis. Mouse cochlear UB/OC-2 cells were treated with BDMC before exposure to gentamicin. The effects of BDMC on hair cell viability, mitochondrial function, and apoptosis-related proteins were examined by flow cytometry, western blot, and fluorescent staining. RESULTS: Our results revealed that BDMC reversed gentamicin-mediated cycle arrest at the G2/M phase, stabilizing the mitochondrial membrane potential, decreasing cleaved caspase proteins, and successfully reversing hair cell apoptosis. CONCLUSION: BDMC is a potential agent for reducing gentamicin-induced ototoxicity.