Both genetic and pharmacologic Jnk loss of function inhibits all the effects of LTB4 to induce cellular insulin resistance in isolated hepatocytes and L6 myocytes. Taken together, these results provide a reasonable Gαi/Jnk dependent molecular mechanism for …

2015年2月23日 · Both genetic and pharmacologic Jnk loss of function inhibits all the effects of LTB4 to induce cellular insulin resistance in isolated hepatocytes and L6 myocytes.

2015年4月6日 · LTB4 stimulation of intraperitoneal macrophages promoted phosphorylation of JNK, the degradation of IκB, and increased expression of proinflammatory cytokines. By contrast, Ltb4r1 inhibitor abrogated the chemotaxis of macrophages towards condition media of 3T3-L1 adipocytes containing LTB4.

Directed leukocyte migration is a hallmark of inflammatory immune responses. Leukotrienes are derived from arachidonic acid and represent a class of potent lipid mediators of leukocyte migration. In this review, we summarize the essential steps leading to the production of LTB 4 …

In this regard, they uncovered that the G protein-coupled receptor (Gαi) and c-Jun N-terminal kinases (JNK) activity as the mediators of LTB4/LTB4R1 deleterious effects in obesity. To elucidate the role of Gαi the authors pre-treated myocytes with the Gαi pharmacological inhibitor, pertussis toxin, that resulted in blockade of LTB4 effects ...

2021年11月4日 · Leukotriene B4 (LTB4), a molecule derived from arachidonic acid, is a potent neutrophil chemoattractant. The excessive amount of LTB4 that is combined with its receptor BLT1 can cause chronic low-grade inflammation, aggravating insulin resistance. Berberine (BBR) has been shown to relieve insulin resistance due to its anti-inflammatory properties.

LTB4 stimulation of intraperitoneal macrophages pro-moted phosphorylation of JNK, the degradation of IkB, and increased expression of proinflammatory cytokines. By contrast, Ltb4r1 inhibitor abrogated the chemotaxis of macrophages towards condition media of 3T3-L1 adipo-cytes containing LTB4.

LTB4 strongly induces MCP-1 production in primary human monocytes. This induction is mediated through the BLT1 pathway increasing MCP-1 transcription. Activation of ERK1/2 or JNK MAPK is essential for this induction.

Thus, we explored the effect of LTB4 on Jnk phosphorylation (pJnk), as a readout of Jnk stimulation, and found that LTB4 at two different concentrations promotes higher pJnk levels compared...

2021年9月13日 · Mass spectrometry identified LTB4 (leukotriene B4) as the lipid mediator that was upregulated in the absence of MST1. We found that MST1 phosphorylated 5-LOX (5-lipoxygenase) at its T218 residue, disrupting the interaction between 5-LOX and 5-LOX-activating protein, resulting in a reduction of LTB4 production.