# Thiotaurine Attenuates TNF-α-Induced Inflammation in Human Chondrocytes via NF-κB Pathway Suppression and Thiol-Dependent Persulfidation

## TL;DR

Thiotaurine reduces inflammation in human cartilage cells by suppressing the NF-κB pathway and increasing hydrogen sulfide levels.

## Contribution

Thiotaurine's anti-inflammatory mechanism via persulfidation and NF-κB suppression is newly demonstrated in chondrocytes.

## Key findings

- Thiotaurine reduced TNF-α-induced IL-6, IL-8, and IL-1β expression in chondrocytes.
- Thiotaurine inhibited p65 phosphorylation and nuclear translocation, suppressing NF-κB activation.
- Persulfide levels increased in cells treated with Thiotaurine.

## Abstract

Thiotaurine (2-aminoethane thiosulfonate) is a naturally occurring sulfur-based compound featuring a thiosulfonate group, enabling it to act as a biologically relevant donor of hydrogen sulfide (H2S) through thiol-dependent persulfidation. H2S levels are known to be reduced in individuals with osteoarthritis, where it plays roles in modulating inflammation, oxidative stress, and pain. This study investigated the anti-inflammatory effects of Thiotaurine in human primary chondrocytes exposed to a pro-inflammatory cytokine. Cells were pre-treated with Thiotaurine prior to stimulation with TNF-α, and the expression levels of key interleukins were assessed at both the mRNA and protein levels. TNF-α stimulation led to upregulation of IL-6, IL-8, and IL-1β, which was significantly attenuated by Thiotaurine pre-treatment. Additionally, immunofluorescence analysis showed that Thiotaurine inhibited the phosphorylation and nuclear translocation of p65, indicating suppression of NF-κB pathway activation. Persulfide detection assays confirmed an increase in intracellular persulfide levels following Thiotaurine treatment. In summary, due to its anti-inflammatory activity and ability to release H2S, Thiotaurine emerges as a promising and potentially safe therapeutic option for osteoarthritis and other inflammation-related conditions.