The effectiveness of different neuroprotective agents in facial nerve injury: An experimental study.

OBJECTIVES/HYPOTHESIS: To examine and compare the neuroprotective effects of dexamethasone, oxytocin, and resveratrol administration on regeneration after facial nerve crush injury in a rat model. STUDY DESIGN: Prospective, randomized, controlled animal study. METHODS: A crush-type facial nerve injury was performed on the right side of all rats (injury group [IG]), whereas there was no injury on the left side (sham group [SG]). These main groups were divided into five subgroups: 1) no medicine (control); 2) physiological serum; 3) dexamethasone; 4) oxytocin; and 5) resveratrol (Res) administered (intraperitoneal injection) for 28 days. Functional recovery was evaluated by daily eye-blink reflex and facial electromyography. Nerve-muscle degeneration and regeneration, apoptosis, and intercellular connections were evaluated in histopathological and immunohistochemical examinations. RESULTS: Recovery time of the postinjury eye-blink reflex demonstrated faster recovery in IG+Res when compared with the other subgroups. In peak-to-peak amplitude values, a significant increase was observed in the dexamethasone (P=0.007) and oxytocin subgroups (P=0.004) and was even more apparent in the resveratrol subgroup (P<0.001). Nerve regeneration is apparent in the resveratrol subgroup. Apoptotic changes were evaluated immunohistochemically with TUNEL and Caspase 3 and 6 antibodies staining. Caspase 3 and 6 immunoexpressions of resveratrol and oxytocin subgroups were moderate when compared with dexamethasone subgroup. Except for the resveratrol subgroup, which had an increase in expression, the majority of subgroups were similar to SG in terms of intercellular connections (Connexin 32 and 43). CONCLUSION: Resveratrol leads to the best outcome after facial nerve crush injury in rats when compared with dexamethasone and oxytocin, even though these agents demonstrate a significant improvement in facial nerve regeneration. LEVEL OF EVIDENCE: N/A.

Jak-Stat signaling pathway may play a role in the pathogenesis of cholesteatoma.

PURPOSE: Jak-Stat signaling pathway is one of the major signal transduction cascades which regulates most of the cellular events such as cell proliferation, differentiation, cell migration and apoptosis. This study aims to determine the activity of Jak-Stat signaling pathway in the pathogenesis of cholesteatoma. MATERIALS AND METHODS: Cholesteatoma and skin samples were obtained from 10 patients who underwent tympanomastoidectomy for chronic otitis media with cholesteatoma. Immunohistochemical analysis of cholesteatoma and skin was performed using anti-Jak1, anti-Jak2, anti-Jak3, anti-Stat1, anti-Stat2, anti-Stat3, anti-Stat4 and anti-Stat5 antibodies. The immunoreactivities in cholesteatoma and skin were quantified using H-score measurement and statistical comparison was performed. RESULTS: Jak1, Jak2, Jak3, Stat1 and Stat3 immunoreactivities were not detected in cholesteatoma; in contrast to the skin (129.8; 226.7; 33.0; 66.4;115.9). In addition, when H-score measurements of Stat2, Stat4 and Stat5 immunoreactivities were compared between cholesteatoma (172.8; 166.7; 120.0) and skin (400.0; 284.9; 292.0), statistically significant differences were found (p<0.0001, p<0.0001, p<0.0001). CONCLUSIONS: A remarkable deficiency in the family members of Jak-Stat signaling pathway was demonstrated in cholesteatoma. Therefore, perturbations in Jak-Stat signaling pathway may play a role in the pathogenesis of cholesteatoma.