Thymol mitigates lipopolysaccharide-induced endometritis by regulating the TLR4- and ROS-mediated NF-κB signaling pathways

Feb 23, 2017Oncotarget

Thymol reduces inflammation in the uterus caused by bacterial toxins by controlling immune and stress-related signaling pathways

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Thymol markedly alleviated LPS-induced pathological injury and inflammation in mouse endometritis.

Thymol reduced myeloperoxidase activity and the production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in vivo.
In vitro studies showed that thymol inhibited the expression of TNF-α, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 in a dose-dependent manner.
Thymol treatment inhibited the expression of the Toll-like receptor 4-mediated nuclear factor-κB pathway.
Silencing of TLR4 blocked the activation of the NF-κB pathway.
Thymol also reduced LPS-induced reactive oxygen species production in a dose-dependent manner.

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The purpose of this study was to investigate the effects of thymol on lipopolysaccharide (LPS)-induced inflammatory responses and to clarify the potential mechanism of these effects. LPS-induced mouse endometritis was used to confirm the anti-inflammatory action of thymol in vivo. RAW264.7 cells were used to examine the molecular mechanism and targets of thymol in vitro. In vivo, thymol markedly alleviated LPS-induced pathological injury, myeloperoxidase (MPO) activity, and the production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in mice. Further studies were performed to examine the expression of the Toll-like receptor 4 (TLR4) -mediated nuclear factor-κB (NF-κB) pathway. These results showed that the expression of the TLR4-mediated NF-κB pathway was inhibited by thymol treatment. In vitro, we observed that thymol dose-dependently inhibited the expression of TNF-α, IL-1β, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW264.7 cells. Moreover, the results obtained from immunofluorescence assays also indicated that thymol dose-dependently suppressed LPS-induced reactive oxygen species (ROS) production. Silencing of TLR4 inhibited NF-κB pathway activation. Furthermore, H2O2 treatment increased the phosphorylation of p65 and IκBα, which were decreased when treated with N-acetyl cysteine or thymol. In conclusion, the anti-inflammatory effects of thymol are associated with activation of the TLR4 or ROS signaling pathways, contributing to NF-κB activation, thereby alleviating LPS-induced oxidative and inflammatory responses.

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Thymol mitigates lipopolysaccharide-induced endometritis by regulating the TLR4- and ROS-mediated NF-κB signaling pathways

Abstract

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