Neuroinflammation Mediates Noise-Induced Synaptic Imbalance and Tinnitus in Rodent Models

[InNeedOfHelp]

I wonder do they have some anecdotal evidence of Enbrel providing a benefit

Effects of Tumor Necrosis Factor Blocker on Salicylate-Induced Tinnitus in Mice

In a salicate induced mice model it did.

 

[Frédéric]

It is a pity the article is behind a paywall. Compared to this thread, similar parameters are acute tinnitus, the hypothesis of neuroinflammation, and rodents. Dissimilar parameters are noise-induced tinnitus instead of salicylate-induced tinnitus and Rolipram (an old drug) instead of TNF.

Noisy tinnitus is a common auditory system disease characterized by persistent tinnitus symptoms. The TLR4/NF - κ B/NLRP3 signaling pathway plays an important role in neuroinflammatory response. Select 6 control and 6 noise exposed mice for transcriptome sequencing analysis in the hippocampus, conduct high-throughput data analysis, identify differentially expressed genes, and screen for pathways. Auditory brainstem response (ABR) detection was performed to understand the hearing changes, and the modeling effect was evaluated using the GPIAS% inhibition experiment of auditory startle reflex. Morphological observation of the basement membrane was performed to determine whether the inner hair cells were damaged. Immunohistochemistry and immunofluorescence were used to determine the activation of microglia in the hippocampus of noise induced tinnitus mice. Finally, qPCR and Western Blot were used to detect the expression of TLR4, NF kB, NLRP3, caspase-1, and IL-1 β in the hippocampus of each group of mice. Through high-throughput data analysis, it was found that there was no significant difference in the auditory threshold of the three groups of mice; After 2 h of exposure to 100 dB SPL noise, the GPIAS% of mice decreased significantly compared to before exposure, and membrane construction was successful. After 7 days, the GPIAS% of the drug intervention group increased. After noise exposure, mice developed tinnitus, and hippocampus neuroinflammation. Roflupram can inhibit neuroinflammation and improve tinnitus through the TLR4/NF kB/NLRP3/caspase-1/IL-1 β signaling pathway.

→ Molecular mechanism of Rolupram reducing neuroinflammation in noise induced tinnitus mice through TLR4/NF kB/NLRP3 protein/caspase-1/IL-1 β signaling pathway

 

[annV]

It is a pity the article is behind a paywall. Compared to this thread, similar parameters are acute tinnitus, the hypothesis of neuroinflammation, and rodents. Dissimilar parameters are noise-induced tinnitus instead of salicylate-induced tinnitus and Rolipram (an old drug) instead of TNF.

Noisy tinnitus is a common auditory system disease characterized by persistent tinnitus symptoms. The TLR4/NF - κ B/NLRP3 signaling pathway plays an important role in neuroinflammatory response. Select 6 control and 6 noise exposed mice for transcriptome sequencing analysis in the hippocampus, conduct high-throughput data analysis, identify differentially expressed genes, and screen for pathways. Auditory brainstem response (ABR) detection was performed to understand the hearing changes, and the modeling effect was evaluated using the GPIAS% inhibition experiment of auditory startle reflex. Morphological observation of the basement membrane was performed to determine whether the inner hair cells were damaged. Immunohistochemistry and immunofluorescence were used to determine the activation of microglia in the hippocampus of noise induced tinnitus mice. Finally, qPCR and Western Blot were used to detect the expression of TLR4, NF kB, NLRP3, caspase-1, and IL-1 β in the hippocampus of each group of mice. Through high-throughput data analysis, it was found that there was no significant difference in the auditory threshold of the three groups of mice; After 2 h of exposure to 100 dB SPL noise, the GPIAS% of mice decreased significantly compared to before exposure, and membrane construction was successful. After 7 days, the GPIAS% of the drug intervention group increased. After noise exposure, mice developed tinnitus, and hippocampus neuroinflammation. Roflupram can inhibit neuroinflammation and improve tinnitus through the TLR4/NF kB/NLRP3/caspase-1/IL-1 β signaling pathway.

→ Molecular mechanism of Rolupram reducing neuroinflammation in noise induced tinnitus mice through TLR4/NF kB/NLRP3 protein/caspase-1/IL-1 β signaling pathway

Attached is the full article.

 

[Josh59]

It is a pity the article is behind a paywall. Compared to this thread, similar parameters are acute tinnitus, the hypothesis of neuroinflammation, and rodents. Dissimilar parameters are noise-induced tinnitus instead of salicylate-induced tinnitus and Rolipram (an old drug) instead of TNF.

→ Molecular mechanism of Rolupram reducing neuroinflammation in noise induced tinnitus mice through TLR4/NF kB/NLRP3 protein/caspase-1/IL-1 β signaling pathway

Interesting study, @Frédéric, thank you for posting it.

Do you have any information about their future work? Will they conduct tests on humans in the future?

The researchers mention neuroinflammation. Could we draw a similar connection to Sound Pharmaceuticals and their research into Meniere's disease and neuroinflammation?

 

[Frédéric]

Do you have any information about their future work? Will they conduct tests on humans in the future?

The researchers mention neuroinflammation. Could we draw a similar connection to Sound Pharmaceuticals and their research into Meniere's disease and neuroinflammation?

I'm sorry, but I just came across this publication, so I do not have any further information.

Feel free to contact them.