OBJECTIVE To compare and analyze the clinical efficacy and safety of postauricular versus intratympanic dexamethasone injection in the treatment of sudden sensorineural hearing loss （SSNHL） with all frequency loss. METHODS A retrospective study was conducted on 150 patients with SSNHL with all frequency loss who were treated at the Hospital of Integrated Traditional Chinese and Western Medicine Affiliated to Zhejiang University of Chinese Medicine between June 1， 2020， and May 31， 2025. According to different injection routes， the patients were divided into the intratympanic group （intratympanic injection， n ＝78） and the postauricular group （postauricular injection， n ＝72）. The differences in hearing threshold indicators and auditory outcomes before and after treatment， tinnitus/vertigo indicators， coagulation function indicators before and after treatment， as well as adverse reactions during treatment were compared between the two groups. RESULTS After treatment， both groups demonstrated significant reductions in the mean speech-frequency threshold and the mean hearing threshold compared with baseline （ P ＜0.05）， whereas no statistically significant differences were observed between the two groups （ P ＞0.05）. Therapeutic outcomes varied significantly across different degrees of hearing loss in each group （intratympanic group： P ＝0.005； postauricular group： P ＜0.001）. Moreover， a significant linear trend relationship was observed between the degree of hearing loss and treatment efficacy grades （ P ＜0.001）， indicating that the more severe the hearing loss， the poorer the treatment outcome （ P ＜0.05）. Notably， the intratympanic group demonstrated superior efficacy compared with the postauricular group in patients with severe and profound hearing loss （ P ＜0.05）. Among patients presenting with vertigo prior to treatment， the postauricular group exhibited a significantly higher response rate than the intratympanic group （ P ＜0.05）， while no statistically significant difference was observed between the two groups in patients with tinnitus （ P ＞0.05）. Regarding coagulation parameters， fibrinogen （FIB） levels and activated partial thromboplastin time decreased or shortened significantly follo wing therapy （ P ＜0.05）， whereas thrombin time （TT） and prothrombin time were significantly prolonged （ P ＜0.05）. Moreover， the postauricular group showed lower FIB levels and longer TT values compared with the intratympanic group （ P ＜0.05）. No significant differences were identified between the two groups in the incidence of gastrointestinal reactions， bleeding manifestations， hepatic or renal dysfunction， or allergic reactions （ P ＞0.05）； however， vestibular adverse reactions occurred more frequently in the intratympanic group （ P ＜0.05）. CONCLUSIONS Compared with intratympanic injection， postauricular dexamethasone injection combined with conventional treatment regimens achieved comparable efficacy in overall hearing improvement in SSNHL patients with all frequency loss. However， the postauricular injection shows potential advantages in vertigo relief， enhancing treatment response in patients with varying degrees of hearing loss， regulating of coagulation function， and declucing of vestibular adverse reactions， while the intratympanic injection may be more suitable for patients with severe hearing loss.

Background Oxidative stress is a pathophysiological process of retina,so it is very important to explore a protective way against retinal oxidative stress.Studies determined that extract of ginkgo biloba (EGb) has antioxidant,anti-apoptosis,anti-thrombosis and anti-inflammatory effects,however,the effect of EGb on human Müller cells in oxidative stress is still below understood.Objective This study was to investigate the protection of EGb against oxidative stress of human retinal Müller cells induced by As2O3 in vitro.Methods Human retinal Müllercell line was cultured in DMEM/F12 with 10％ fetal bovine serum (FBS),2 μmol/L glutamine and 1％ antibiotics.As2O3 solution at the final concentration 5 mg/L was added in the medium for 24 hours to establish oxidative models,and then the EGb with the final concentrations of 5,10 and 20 mg/L was used to cell models for 24 hours,respectively.Cell viability was detected by MTT assay,and reactive oxygen species (ROS) levels in the cells were detected with CM-H2DCFDA fluorescent probe.The relative expression levels of caspase-3 mRNA in cytoplasm and cell nuclei were assayed by reverse-transcription PCR (RT-PCR),and the expressions of Nrf2 protein were quantitatively detected by Western blot.Results Müller cells adhered well 24 hours after cultured.At 6-7 days after culture,Müller cell body was large with abundant cytoplasm and mosaic-like arrangement.However,floating cells were seen after As2 O3 treatment.Cell viability (absorbance) was significantly different among the normal culture group,As2 O3-treated group,As2 O3 + 5 mg/L EGb group,As2 O3 + 10 mg/L EGb group and As2 O3 + 20 mg/L EGb group,with the strongest viability in the normal culture group and the weakest viability in the As2 O3-treated groups (F=163.57,P =0.00).The fluorescence intensity of ROS was the weakest in the normal culture group and the strongest in the As2 O3-treated group and was gradually weakened with the increase of EGb doses,showing a remarkable difference among the groups (F =4 013.61,P =0.00).The relative expression level of caspase-3 mRNA in the cells was gradually reduced with the increase of EGb doses,with a statistically significant difference among the groups (F =2 199.72,P =0.00).In addition,no considerable difference was seen in the expression level of Nrf2 protein (grey scale) in cytoplasm among the groups (F=15.42,P=0.40);while in the nuclei,the expression levels of Nrf2 protein were 100.01 ±0.04,46.59±0.63,54.51 ±0.62,59.93 ±0.17 and 67.60±0.24 in the normal culture group,As2 O3-treated group and As2O3+5 mg/L EGb group,As2O3+10 mg/L EGb group,As2O3+20 mg/L EGb group respectively,with a significant difference among them (F=7 271.72,P=0.00).Conclusions EGb can protect human retinal Müller cells against As2O3-induced damage in a dose-dependant manner by antioxidant and antiapoptotic effects in vitro,and the activities occur primarily in cell nucleus.

Background Oxidative stress is a main cause of age-related macular degeneration (AMD).Lutein has a preventive role for AMD, but its antioxidant mechanism remains unclear.Objective Present study was to investigate the effect of lutein on oxidative stress of Müller cells and its signaling pathway.Methods Human Müller cells (human Müller cell strain) were cultured, and the cells at logarithmimic growth phase were incubated in 96 well plate overnightly.Oxidative stress cell models were established by adding 160 μmol/L H2O2, a median lethal dose for Müller cells.The models were divided into the model control group and 12.5,25.0,50.0 mg/L lutein groups,and the different concentrations of lutein were used to culture the cells for 24 hours, respectively.The routine cultured cells served as the blank control group.Growth of the cells was assayed by MTT method (absorbancy);the reactive oxygen species (ROS) content in the cells was assayed by flow cytometry;the mRNA and protein levels of nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the cells were detected by quantitative real-time PCR and Western blot, respectively.Results The inhibitory effects on the cells were gradually enhanced with the increase of H2O2 concentrations,showing a significant difference among the groups (F =43.890,P＜0.01).A significant difference was found in apoptotic rate of the cells among the blank control group,model control group and 12.5,25.0,50.0 mg/L lutein groups (F =346.770, P =0.000) , and the apoptosis rate was significant elevated with the increase of lutein dose (all at P＜0.05).The ROS contents in the cells were 1.92±0.18,64.89±2.86,52.70±2.80,32.61 ±4.20 and 5.68 ± 1.35 in the blank control group, model control group and 12.5,25.0,50.0 mg/L group, respectively, with significant difference among the groups (F =324.900, P =0.000), and the ROS content was gradually reduced as the increase of lutein dose (all at P＜0.05).The relative mRNA and protein expressions of Nrf2 and HO-1 were remarkedly higher in the 12.5,25.0,50.0 mg/L lutein groups than those in the model control group (F =236.960,242.620,186.830,263.120, all at P =0.000) , and no significant difference was seen in the relative expression level of nuclear Nrf2 protein among the groups (F =1.790, P =0.210).Conclusions Lutein can induce the expression of antioxidant enzymes by inducing the expression of nuclear translocation of Nrf2 and consequently inhibit the oxidative stress status.