Inhibition of NF-κB activation by diethylcarbamazine prevents alcohol-induced liver injury in C57BL/6 mice

Gypsophila elegans isoorientin attenuates CCl4-induced hepatic fibrosis in rats via modulation of NF-κB and TGF-β1/Smad signaling pathways

“…Moreover, CCl 4 -induced liver fibrosis was associated with a marked activation of Smad2/3 but a loss of Smad7, suggesting that the imbalance between Smad2/3 and Smad7 signaling could be important in the pathogenesis of liver fibrosis. This is confirmed by the recent studies that overexpression of Smad7 in the liver attenuates TGF-β/Smad signaling and protects against HSC activation and liver fibrogenesis in CCl 4 -induced mouse and rat models [10,11]. Our results showed that GEI treatment was able to inhibit the phosphorylation of Smad2/3 and reversed the inhibitory effect of CCl 4 treatment on Smad7 expression.…”

“…It is activated by oxidants and cytokines such as interleukin-1β (IL-1β) and cytokine tumor necrosis factor-α (TNF-α) [10]. Activation of NF-κB occurs mainly through phosphorylation and thereby degradation of the inhibitory molecule IκBα, releasing the cytosolic dimer NF-κB p65/p50 to translocate into the nucleus and bind to DNA to stimulate the transcription of genes including TGF-β and intercellular adhesion molecule-1 (ICAM-1).…”

Diethylcarbamazine citrate ameliorates insulin resistance in high-fat diet-induced obese mice via modulation of adipose tissue inflammation

“…However, other doses could show also inhibitive effect. This finding was also observed in previous studies on DEC antiinflammatory action [10,11]. This confirms the inhibitive action of DEC on intracellular signaling pathways which interfere with insulin-receptor signaling.…”

“…It inhibits prostaglandins for the clearance of blood microfilariae [9]. DEC has been known as an anti-inflammatory drug because of its success to reduce the experimentally induced inflammation in lung and liver [10,11]. These reduced inflammatory responses could be attributed to the inactivation of NF-κB and thus suppressing the induction of NF-κB-dependent genes.…”

Anti-inflammatory function of ginsenoside Rg1 on alcoholic hepatitis through glucocorticoid receptor related nuclear factor-kappa B pathway

“…GR is a sort of antiinflammatory factor inhibiting resultant inflammatory reaction, which primarily through its modulatory influence on nuclear factor-kappa B (NF-κB) (Lavrovsky et al, 2000). NF-κB activation is implicated in the pathogenesis of a number of inflammatory diseases (Lavrovsky et al, 2000), because it could be activated by cytokines (Barnes and Karin, 1997), which play important roles in inflammation and the development of AH (da Silva et al, 2014). Steroids hold favorable anti-inflammatory effects, however, long term use could cause serious side reactions, even inducing or aggravating infections.…”