Plasma cytokine concentrations increased profoundly during endotoxaemia (control group: tumor necrosis factor alpha [TNF-α] from 14 [9-16] pg ml<sup>-1</sup> at baseline to 480 [284-709] pg ml<sup>-1</sup> at 1.5 h after LPS; interleukin-6 [IL-6] from 4 [4-4] pg ml<sup>-1</sup> at baseline to 659 [505-1018] pg ml<sup>-1</sup> at 2 h after LPS).
The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation.
LAH also significantly reduced the concentration of tumour cell necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in both serum and colon and decreased the level of lipopolysaccharides (LPS) in serum and feces, leading to reduced systematic inflammation and metabolic endotoxemia.
20TT in the heat increased I-FABP and elevated inflammatory cytokines (IL-6 and TNF-α) compared to pre-exercise values but did not result in endotoxemia.
In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice.
It alleviated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in activated macrophages by downregulating the NF-κB activity, and it reduced the mortality rate in LPS induced endotoxemia mice.
At postoperative day 7, the sepsis-positive group continued to demonstrate an increase in intestinal permeability, endotoxemia and elastase; a significant difference was observed between the two groups (P = 0.02), whereas there was no significant difference in IL-1, IL-6, and CRP levels.
In addition, it resulted in the reduction of endotoxemia (through lipopolysaccharides (LPSs)) and pro-inflammatory cytokine (tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and interleukin 1β (IL-1β)) levels, with the increased expression of tight-junction associated proteins (claudin-1, occludin, and zonula occludens-1).
Furthermore, leptin pre-treatment decreased the oxidative stress burst in blood and blunted the increased pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 observed during endotoxemia.
Furthermore, therapeutic studies in a systemic endotoxemia model demonstrated that mSPAM treatment reduced TNF-α and IL-6 inflammatory cytokines in serum, in turn circumventing organ damage done by the inflammatory macrophages.
Treatment with both AGE and RGE in an in vivo experiment of LPS-induced endotoxemia significantly reduced the level of TNF-α and interleukin-6 in serum and completely protected against LPS-induced lethal shock in C57BL/6 mice.
300 min after the proinflammatory insult, plasma concentrations of IL-1β and IL-6 in the plasma remain considerably lower after CLI compared to endotoxemia.
Reciprocal regulation of IL-6 and IL-10 balance by HGF via recruitment of heme oxygenase-1 in macrophages for attenuation of liver injury in a mouse model of endotoxemia.