Protective effects of the suppressed NF‐κB/TLR4 signaling pathway on oxidative stress of lung tissue in rat with acute lung injury

Abstract

The pathogenesis of acute lung injury (ALI) is characterized by lung inflammation and lung oxidative stress. The study was conducted in order to investigate the effect toll‐like receptor 4 (TLR4) and nuclear factor‐kappa B (NF‐κB) exhibited on oxidative stress in ALI. After the rats had been assigned into different groups, arterial blood, white blood cell (WBC), lung permeability index (LPI), wet/dry (W/D) ratio, TLR4 and NF‐κB expression and superoxide dismutase (SOD), myeloperoxidase (MPO), malondialdehyde (MDA), glutathione (GSH), and reactive oxygen species (ROS) were examined. Afterward, the correlation between the levels of TLR4 and NF‐κB was determined. Decreased levels of PaO2, SOD, MPO, and GSH accompanied by increased levels of PaCO2, WBC number, LPI and W/D ratio, MDA and ROS, as well as TLR4 and NF‐κB expressions in the ALI, ALI + NF‐κB inhibitor, and ALI + phosphate buffer saline groups were found. Inhibition of NF‐κB resulted in increased PaO2 and decreased PaCO2 levels, WBC number, and LPI and W/D ratio. Decreased expression of NF‐κB increased SOD, GSH, and MPO, but decreased MDA and ROS. We also found that NF‐κB inhibition resulted in the improvement of ALI in rats. TLR4 and NF‐κB expressions were negatively correlated with levels of SOD, MPO, and GSH, and positively correlated with MDA and ROS levels. In summary, our findings provided evidence that inhibition of the TLR4/NF‐κB signaling pathway decreases oxidative stress, thereby improving ALI. As a result, NF‐κB signaling pathway has shown potential as a therapeutic target in ALI therapy.

Gut-Lung Dysbiosis Accompanied by Diabetes Mellitus Leads to Pulmonary Fibrotic Change through the NF-κB Signaling Pathway

“…The destruction of the intestinal flora causes bacterial translocation, activates the lung immune response, induces the production of a large number of inflammatory factors, triggers oxidative stress, and subsequently damages the lung tissue. 70 FMT may reduce the oxidative damage and enhance the antioxidant capacity. Therefore, the imbalance of the intestinal flora increases the immune response to the bacteria in the lungs through the gut-lung axis and activates the oxidative stress in the lungs.…”

Lycorine attenuates lipopolysaccharide-induced acute lung injury through the HMGB1/TLRs/NF-κB pathway

“…Thus, the NF-κB pathway is critical for the induction of inflammatory response and oxidative stress. Additionally, the early studies showed that the blockade of TLR4/NF-κB pathway effectively inhibited oxidative stress and inflammatory responses in the lungs (Deng et al 2017 ; Zhang et al 2019 ). Therefore, the HMGB1/TLR4/NF-κB pathway is an important pathway to induce inflammatory response and oxidative stress.…”

Bupleurum chinense Polysaccharide Improves LPS-Induced Senescence of RAW264.7 Cells by Regulating the NF-κB Signaling Pathway

“…NF- κ B is an important transcription factor ubiquitous in the central nervous system and a key transcription factor involved in oxidative stress and the inflammatory response [ 45 ]. The NF- κ B signaling pathway is involved in inhibition of oxidative stress-induced cell damage [ 46 ]. p65 and I- κ B α have been identified as indicators for detection of the NF- κ B signaling pathway.…”