Budesonide (Pulmicort), an anti-inflammatory corticosteroid, has shown the effective glucocorticoid activitie and few mineralocorticoid activities. According to reports, Budesonide has extensively inhibitory effects against multiple cells types and mediators referred to allergic and nonallergic-mediated inflammatory. What's more, the anti-inflammatory action of budesonide has been revealed to contribute to the effectiveness of asthma.

Budesonide 能有效抑制依他命素和RANTES蛋白的产生，且Budesonide 对人支气管上皮细胞系BEAS-2B和原代人支气管上皮细胞中趋化因子mRNA的表达有不同程度的抑制作用。Budesonide 可抑制人支气管上皮细胞系 BEAS-2B 和原代人支气管上皮细胞中 RANTES 和 eotaxin 启动子驱动的报告基因活性。Budesonide 还能选择性地促进人支气管上皮细胞系 BEAS-2B 和原代人支气管上皮细胞中 eotaxin 和 MCP-4 mRNA 的衰减。[1]Budesonide 在时间和蛋白质合成方面依赖性地减少了两种细胞类型中血管内皮生长因子的分泌和血管内皮生长因子 mRNA 的表达，而这些作用被糖皮质激素受体拮抗剂米非司酮（RU 486）所抑制，这表明Budesonide 通过其糖皮质激素受体介导的作用减少了血管内皮生长因子的分泌和表达。[2]Budesonide 对猪粉尘诱导的上皮细胞 IL-6 和 IL-8 以及 LPS 诱导的肺泡巨噬细胞 IL-6 和 TNF-α 的释放有剂量依赖性抑制作用。[3]

Budesonide 在低浓度（2.5 mg/mL/kg）和高浓度（50 mg/mL/kg）的情况下，可完全阻止大鼠在接受 LPS 挑战后 TNF-α、白细胞介素（IL）-1beta、IL-6 和单核细胞趋化蛋白（MCP）-1 的产生。[4] Budesonide 通过Mad2/3抑制生长，通过Bim/Blk和推断的caspase-8/9导致细胞凋亡，从而在A/J小鼠中发挥化学预防作用。[5]

Biochemical assays: Recombinant baculoviruses expressing Raf-1 (residues 305–648) and B-Raf (residues 409–765) are purified as fusion proteins. Full-length human MEK-1 is generated by PCR and purified as a fusion protein from Escherichia coli lysates. Sorafenib tosylate is added to a mixture of Raf-1 (80 ng), or B-Raf (80 ng) with MEK-1 (1 μg) in assay buffer [20 mM Tris (pH 8.2), 100 mM NaCl, 5 mM MgCl2, and 0.15% β-mercaptoethanol] at a final concentration of 1% DMSO. The Raf kinase assay (final volume of 50 μL) is initiated by adding 25 μL of 10 μM γ[33P]ATP (400 Ci/mol) and incubated at 32 °C for 25 minutes. Phosphorylated MEK-1 is harvested by filtration onto a phosphocellulose mat, and 1% phosphoric acid is used to wash away unbound radioactivity. After drying by microwave heating, a β-plate counter is used to quantify filter-bound radioactivity. Human VEGFR2 (KDR) kinase domain is expressed and purified from Sf9 lysates. Time-resolved fluorescence energy transfer assays for VEGFR2 are performed in 96-well opaque plates in the time-resolved fluorescence energy transfer format. Final reaction conditions are as follows: 1 to 10 μM ATP, 25 nM poly GT-biotin, 2 nM Europium-labeled phospho (p)-Tyr antibody (PY20), 10 nM APC, 1 to 7 nM cytoplasmic kinase domain in final concentrations of 1% DMSO, 50 mM HEPES (pH 7.5), 10 mM MgCl2, 0.1 mM EDTA, 0.015% Brij-35, 0.1 mg/mL BSA, and 0.1% β-mercaptoethanol. Reaction volumes are 100 μL and are initiated by addition of enzyme. Plates are read at both 615 and 665 nM on a Perkin-Elmer VictorV Multilabel counter at ~1.5 to 2.0 hours after reaction initiation. Signal is calculated as a ratio: (665 nm/615 nM) × 10,000 for each well. For IC50 generation, Sorafenib tosylate is added before the enzyme initiation. A 50-fold stock plate is made with Sorafenib tosylate serially diluted 1:3 in a 50% DMSO/50% distilled water solution. Final Sorafenib tosylate concentrations range from 10 μM to 4.56 nM in 1% DMSO.