Anti-inflammatory effect of SQC-β-CD on lipopolysaccharide-induced acute lung injury

Astragalin-induced cell death is caspase-dependent and enhances the susceptibility of lung cancer cells to tumor necrosis factor by inhibiting the NF-κB pathway

“…The activated NF-κB heterodimers then binds to consensus sequences activating expression of target genes [48]. LPS, a component of the Gram-negative bacterial cell wall, can induce strong proinflammatory response in cells and animals [49]. The binding of LPS to its receptor TLR4 results in the activation of IKK, the subsequent degradation of IκBα and NF-κB activation.…”

Asiaticoside attenuates lipopolysaccharide-induced acute lung injury via down-regulation of NF-κB signaling pathway

“…However, these clinical trials have, thus far, been unsuccessful [19]. LPS is the major constituent of the outer cell wall of Gram-negative bacteria and the predominant inducer of inflammatory responses to these bacteria [20]. LPS-induced ALI was characterized by the disruption of endothelial and epithelial integrity, lung edema, the release of inflammatory mediators, and extensive neutrophil infiltration [21].…”

“…The cells were pretreated with different concentrations(10,20 or 40 mg/L) of AS for 1 h prior to stimulation with 4 mg/L of LPS for 24 h. The production of TNF-α (A) and IL-6 (B) in the culture supernatant of macrophages was measured by ELISA kits. (C) The phosphorylation and degradation of IκB were tested by Western blot with specific antibodies as described.…”

Fucosterol attenuates lipopolysaccharide-induced acute lung injury in mice

“…Uncontrolled inflammatory cytokines cause tissue injury and severe immunopathology. Inhibition of these cytokines could alleviate pulmonary injury [20]. To investigate the protective and treatment mechanism of fucosterol, the effects of fucosterol on inflammatory cytokines were detected.…”