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Conclusion:The results showed a gradual detachment of otoconia in the utricle after a single event of head vibration, possibly explaining the frequent recurrence of BPPV attacks and persistent dizziness after trauma. Objectives:This study developed a murine model of traumatic BPPV and observed the changes in otoconia detachment over time. Methods:Six-week-old CBA mice were used in this study. Otoconia detachment was induced by vibrating the head for 2 min. Utricles of mice were harvested from different groups: before the head vibration and 1 day, 1 week, 1 month, and 3 months after vibration application. Using scanning electron microscopy and ImageJ software, the percentage of the intact area of otoconia in the utricle was calculated. Hearing thresholds were compared among the groups. Results:The mean (± SD) percentages of the intact area of otoconia in the utricle were 98.1% ± 1.7% before the vibration and 93.6% ± 1.7%, 88.9% ± 5.3%, 78.2% ± 20.9%, and 38.9% ± 24.1% at 1 day, 1 week, 1 month, and 3 months after the vibration, respectively. The percentage decreased significantly over time after the vibration (p < .001). The hearing thresholds were not different among the groups. [ABSTRACT FROM PUBLISHER]

Dendropanax morbifera ( D. morbifera), a species endemic to Korea, is largely distributed throughout the southern part of the country. Its leaves, stems, roots, and seeds have been used as a form of alternative medicine for various diseases and neurological disorders including paralysis, stroke, and migraine. However, the molecular mechanisms that underlie the remedial effects of D. morbifera remain largely unknown. In this paper, extracts from D. morbifera leaves were prepared using ethyl acetate as a solvent (abbreviated as DMLE). The modulatory effects of DMLE on neuroinflammation were studied in a lipopolysaccharide (LPS)-stimulated BV2 murine microglial cell line. Production of pro-inflammatory cytokines, activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-B), and different M1/M2 activation states of microglia were examined. DMLE treatment suppressed the production of pro-inflammatory cytokines including tumor necrosis factor- (TNF-), interleukin-6 (IL-6), and nitric oxide (NO) in LPS-stimulated BV2 cells. DMLE treatment also attenuated the activation of MAPKs and NF-B. In a novel discovery, we found that DMLE up-regulated the marker genes representing an alternative, anti-inflammatory M2 polarization, while suppressing the expression of the classical, pro-inflammatory M1 activation state genes. Here, we uncovered the cellular mechanisms underlying the beneficial effects of D. morbifera against neuroinflammation using BV2 microglia cells. These results strongly suggest that DMLE was able to counter the effects of LPS on BV2 cells via control of microglia polarization states. Additionally, study results indicated that DMLE may have therapeutic potential as a neuroinflammation-suppressing treatment for neurodegenerative diseases. [ABSTRACT FROM AUTHOR]