Fig. 6: Pharmacological inhibition of SGK1 increases the severity of LPS-induced EH and audiovestibular symptoms in vivo.

a–i The WT mice were untreated or pretreated with GSK650394 and challenged with LPS or saline. a Representative images of mid-modiolar cochlear sections, scale bar = 200 μm. b Measurements of IR-L in cochlear half-turns I–IV (n = 5 mice per group). c Representative serial ABR wave recordings and thresholds in response to click sounds (n = 5 mice per group). d ABR thresholds in response to pure tone burst across all frequencies tested (4, 8, 12, 16, 24, and 32 kHz) (n = 5 mice per group). *P indicates p-values for GSK650394 + LPS versus LPS; ^#P indicates p-values for GSK650394 + LPS versus GSK650394; ^†P indicates p-values for LPS versus Control. e Representative click-evoked VEMPs waves, P1-N1 peak amplitudes, and the P1 (white triangle) and N1 (black triangle) peak latencies of VEMPs at 100 dB nHL (n = 5 mice per group). f Quantification of rotarod test (n = 5 mice per group). g ELISA for plasma Casp-1 and IL-1β levels (n = 3 mice per group). h Western blot analysis showing NLRP3, SGK1, pro Casp1, Casp-1 p20, pro IL-1β and cleaved IL-1β levels in inner ears (n = 3 mice per group). i Immunofluorescence staining for TUNEL (green) and Myosin VIIa (red) in the basilar membrane, scale bar = 50 μm. Results are presented as mean ± SD. Statistical analyses were carried out via one-way ANOVA for b, c, e–g, and two-way ANOVA for d. EH endolymphatic hydrops, IR-L Increase ratios (IR) of the length of the Reissner’s membrane, ABR auditory brainstem response, VEMPs vestibular-evoked myogenic potentials, P1 positive peak, N1 negative peak, Casp-1 caspase-1. Source data are provided as a Source Data file.