17-HDHA

17-HDHA (10-20 nM) potently inhibits PDGFbb-induced proliferation of mouse pulmonary artery smooth muscle cells^[2].
17-HDHA inhibits the adhesion and migration of neutrophils to monocytes/macrophages by activating formyl peptide receptor 2 (FPR2)^[2].
17-HDHA (10 nM; 24 h) activates PPARγ nuclear translocation and inhibits PDGFbb-stimulated Stat3 phosphorylation in mouse pulmonary artery smooth muscle cells^[2].
17-HDHA (10-100 nM; 6 days) significantly reduces spontaneous and stimulus-induced IgE production in peripheral blood mononuclear cells from asthmatic patients not receiving oral corticosteroids^[3].
Pretreatment with Dexamethasone (HY-14648) blocks the inhibitory effect of 17-HDHA (10-100 nM; 6 days) on IgE production in peripheral blood mononuclear cells from asthmatic patients not receiving oral corticosteroids^[3].
17-HDHA (10-100 nM; 24-72 h) reduces IgE production, ε germline transcript levels and mature IgE mRNA levels in purified CD19⁺ B cells from healthy donors, and pretreatment with Dexamethasone blocks these inhibitory effects^[3].
The ability of 17-HDHA (10-100 nM; 7 days) to reduce IgE production in purified CD19⁺ B cells and peripheral blood mononuclear cells from healthy donors is blocked by the 5-lipoxygenase inhibitory effect of zileuton^[3].
17-HDHA (10-100 nM; 6 days) enhances Dexamethasone-induced PPARγ binding activity in purified CD19⁺ B cells from healthy donors, but exerts no effect on PPARγ binding activity when used alone^[3].
17-HDHA (10-100 nM; 4 h) enhances the expression of Bcl-6 protein in purified CD19⁺ B cells derived from healthy donors, and pretreatment with Dexamethasone reduces Bcl-6 expression regardless of 17-HDHA treatment^[3].
17-HDHA (10-100 nM; administered daily for 6 consecutive days, with 30 min pre-incubation prior to stimulation) upregulates the expression of CD80 and CD86 on purified naive CD19⁺ B cells from C57BL/6 mice activated by CpG combined with anti-IgM, without altering the expression of MHC class II^[4].
17-HDHA (10-100 nM; administered daily for 6 consecutive days, with 30 min pre-incubation prior to stimulation) enhances the production of IgM and IgG in purified naive CD19+ B cells from C57BL/6 mice activated by CpG combined with anti-IgM, and upregulates the mRNA and protein levels of Blimp-1^[4].
17-HDHA (10-100 nM; 4 h) enhances the binding of Bcl-6 to the promoter region of εGLT in peripheral blood mononuclear cells from healthy donors, while pretreatment with Dexamethasone blocks this enhancing effect^[3].
17-HDHA (10-100 nM; administered daily for 5-6 days, with 30 min pre-incubation prior to stimulation) promotes the differentiation of naive CD19⁺CD138⁻ B cells from plasma cell-depleted C57BL/6 mice into IgM⁻ secreting cells, IgG-secreting cells and plasmablasts, increases IL-10 production, and exerts no effect on cell proliferation or the production of IL-6/TNF-α^[4].
17-HDHA (0.4-50 μM; 48 h during viral infection) does not inhibit the replication of pH1N1/E3 influenza virus in MDCK cells at the highest concentration^[4].
17-HDHA (5-25 μM; 10 min) inhibits collagen-induced aggregation of washed human platelets at a concentration of 5 μM, inhibits thrombin-induced aggregation of washed human platelets at a concentration of 25 μM, and exhibits no agonist activity^[5].
17-HDHA (300-1000 nM; 4-24 h) induces elevated levels of specific D-series resolvins and 10S,17S-dihydroxydocosahexaenoic acid (10S,17S-diHDHA) in human primary great saphenous vein endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). Moreover, starting from treatment with 300 nM 17-HDHA, the production of RvD1 shows concentration- and time-dependent patterns^[6].
17-HDHA (1 μM; 24 h) increases 5-LOX protein expression by 94% in primary human great saphenous vein endothelial cells (but not in vascular smooth muscle cells)^[6].
17-HDHA (1 μM; 5 h) induces the translocation of 5-LOX from the nucleus to the cytoplasm in primary human great saphenous vein endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), with the relative cytoplasmic 5-LOX expression levels increasing by 28% and 37% in ECs and VSMCs, respectively^[6].
Conditioned medium generated from human primary great saphenous vein endothelial cells (ECs) treated with 17-HDHA (1 μM; 24 h) attenuates the adhesion of TNF-α-stimulated U937 monocytes to ECs, and this effect is partially mediated by RvD1 signaling via ALX/FPR2 and GPR32 receptors^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.