Acetylbritannilactone suppresses lipopolysaccharide-induced vascular smooth muscle cell inflammatory response

作者：Liu Yue Ping; Wen Jin Kun; Zheng Bin; Zhang Di Qun; Han Mei^*

来源：European Journal of Pharmacology, 2007, 577(1-3): 28-34.

DOI：10.1016/j.ejphar.2007.08.030

• 1-O-acetylbritannilactone
• nuclear factor-kappa B
• vascular smooth muscle cell
• cyclooxygenase-2

To investigate the mechanism of action by which a new anti-inflammatory active compound, 1-O-acetylbritannilactone (ABL) isolated from Inula britannica-F, inhibits inflammatory responses in vascular smooth muscle cells (VSMCs). Enzyme immunoassay was used to measure the levels of prostandin E-2 (PGE(2)) production. Immunocytochemistry staining and Western blot analysis were performed to detect the nuclear translocation of nuclear factor-kappa B (NF-kappa B) p65 and the expression Of I kappa B-alpha, p kappa B-alpha and cyclooxygenase-2 (COX-2). Electrophoretic mobility shift assays (EMSA) were used to detect DNA-binding activity of NF-kappa B in VSMCs. ABL (5, 10, 20 mu mmol/l) had several concentration-dependent effects, including inhibition of lipopolysaccharide (LPS)-induced PGE(2) production and COX-2 expression, and blockade of NF-kappa B activation and translocation. These effects were owing to reductions in I kappa B-alpha phosphorylation and degradation induced by LPS. In addition, ABL directly inhibited the binding of active NF-kappa B to specific DNA cis-element. These results indicate that ABL is a potent inhibitor of LPS-stimulated VSMC inflammatory responses through blockade of NF-kappa B activity and inhibition of inflammatory gene COX-2 expression.

• 出版日期2007-12-22
• 单位河北医科大学