| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | HEK-Blue cells,RAW macrophages,THP-1 macrophages |
Preparation Method | C29 were dissolved in DMSO as 50mM stock solution. Final DMSO concentrations in cell culture were below 0.2% (v/v). The cells were first incubated with the C29 for 1h and afterwards stimulated with the respective TLR(Toll like receptor) agonist. |
Reaction Conditions | 0.01µM, 0.1µM, 1µM, 10µM 100µM for 1 hour |
Applications | C29 showed inhibit affection for TLR2/1 or TLR2/6 (IC50 21µM and 23µM). |
Animal models | Female C57BL/6J mice |
Preparation Method | C29 was dissolved and diluted in solution (10% DMSO/40% PEG300/5% Tween-80/45% saline), then injected intraperitoneally (1.3 µmol/g) 1 h before HBeAg treatment, with the same volume of dissolving reagent as the vehicle group. |
Dosage form | Intraperitoneal injection, 1.3 µmol/g |
Applications | To verify the roles of TLR-2 in vivo, mice were pretreated with C29 before the administration of HBeAg. The expression of IL-6, TNF-α, and CCL-2 was significantly alleviated, but IL-10 was upregulated in the liver. |
| 文献引用 | |
| 产品描述 | C29 is a Toll-like receptor 2 (TLR2) inhibitor. C29, inhibited TLR2/1 and TLR2/6 signaling induced by synthetic and bacterial TLR2 agonists in human HEK-TLR2 and THP-1 cells, but only TLR2/1 signaling in murine macrophages. C29 failed to inhibit signaling induced by other TLR agonists and TNF-α. Mutagenesis of BB loop pocket residues revealed an indispensable role for TLR2/1, but not TLR2/6, signaling, suggesting divergent roles[1]. C29 inhibited TLR2/1-mediated NF-κB activation (IC500.87μM), and inhibited TLR2/6 heterodimer with IC5023μM[2]. C29 and o-vanillin may function by specifically targeting the BB loop pocket of the TLR2 TIR domain, altering its function and/or position[1]. Mice were pretreated with C29 before the administration of hepatitis B e antigen (HBeAg), to verify the roles of TLR-2 in vivo, the expression of IL-6, TNF-α, and CCL-2 was significantly alleviated, but IL-10 was upregulated in the liver[3]. C29 did not affect lipid accumulation, but the adipogenesis inhibitory effects of exopolysaccharide (EPS) significantly decreased in the C29-treated group. The results showed that activation of the AMPK signalling pathway by EPS was inhibited in the early stage (day 4) of adipogenic differentiation, when TLR2 and myeloid differentiation primary response 88 (MyD88) expression is inhibited by C29, indicating that EPS activates the AMPK signalling pathway by interacting with TLR2, consequently inhibiting adipogenesis[4]. References: |
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