No abstract

Introduction: Hearing loss is one of the most common sensory disorders. Recent findings have shown that the apoptotic program and autophagy are related to hearing loss. The aim of study was to explore the effects of noise and cisplatin exposure on apoptosis and autophagy in the hair cells of the cochleae. Material and methods: C57BL/6 mice were randomly divided into 3 groups (n = 10 for each): the control group, the noise model group and the cisplatin model group. Auditory brainstem response (ABR) measurements were used to detect the hearing thresholds. TUNEL assay was used to evaluate cell apoptosis. Western blot and immunofluorescence were performed to examine the apoptosis-and autophagy-related proteins. Results: The mice exhibited substantial hearing loss after noise and cisplatin exposure. Additionally, more TUNEL positive cells were observed in the mice after noise and cisplatin exposure compared with the control group. Moreover, the protein expression levels of Beclin-1, LC3-II, Bax and cleaved caspase-3 were significantly increased, while the expression of Bcl-2 was notably decreased in the cochlea after noise (p = 0.0278, 0.0075, 0.0142, 0.0158, 0.0131 respectively) and cisplatin (p = 0.0220, 0.0075, 0.0024, 0.0161, 0.0452 respectively) exposure compared with the control group. Besides, the ratio of LC3-II/LC3-I was substantially higher in the mice treated by cisplatin (p = 0.0046) and noise (p = 0.0220) compared with the control group. Conclusions: Our findings demonstrated for the first time that noise and cisplatin exposure promoted apoptosis and autophagy in the hair cells of the cochleae. This study provides new insights into the mechanisms of noise-or cisplatin-induced hearing loss.

Purpose: Aiming at measuring levels of High-mobility group box-1 (HMGB1) and inflammation-related cytokines in the aqueous humor of patients with acute primary angle-closure glaucoma (APAG) and age-related cataract eyes (ARC). Methods: Aqueous humor samples were obtained from 59 eyes of 59 Chinese subjects(APAG, 32 eyes; and ARC, 27eyes). The multiplex bead immunoassay technique was used to measure the Levels of HMGB1 and IL-8, IL-6, G-CSF, MCP-3, VEGF, sVEGFR-1, sVEFGR-2, TNF-α, PDGF and IL-10 in aqueous. The data of Patients’ demographics and preoperative intraocular pressure (IOP) were also gathering for related analysis. Results: The APAG group showed significantly elevated concentrations of HMGB1, IL-8, IL-6, G-CSF, VEGF, sVEGFR-1 and TNF-α than those in ARC group. Aqueous HMGB1 level correlated significantly with IOP, IL-8, IL6, G-CSF and sVEGFR-1 levels but not with age, TNF-α or VEGF levels. Conclusions: The aqueous level of HMGB1 is elevated in APAG and is associated with aqueous level of inflammation-related cytokines, suggesting an association between elevated levels of HMGB1, APAC and certain inflammatory modulators which, of course, should lead to further investigations in order to demonstrate cause and effect.

No abstract

No abstract