| Catalogue number | C101757 |
| Chemical name | Sphondin |
| CAS Number | 483-66-9 |
| Synonyms | 6-methoxy-2-furo[2,3-h][1]benzopyranone |
| Molecular Weight | C12H8O4 |
| Formula | 216.2 |
| Purity | 98% |
| Physical Description | Powder |
| Solvent | Chloroform, Dichloromethane,DMSO |
| Storage | Stored at 2-8°C, Protected from air and light, refrigerate or freeze |
| Applications | Sphondin possessed an inhibitory effect on IL-1beta-induced increase in the level of COX-2 protein and PGE(2) release in A549 cells. Pretreatment of cells with sphondin (10-50 microM) concentration-dependently attenuated IL-1beta-induced COX-2 protein expression and PGE(2) release. The IL-1beta-induced increase in COX-2 mRNA expression was also attenuated by sphondin (50 microM). The selective COX-2 inhibitor, NS-398 (0.01-1 microM), inhibited the activity of the COX-2 enzyme in a concentration-dependent manner, while sphondin (10-50 microM) had no effect. Sphondin (50 microM) did not affect the IL-1beta-induced activations of p44/42 MAPK, p38 MAPK, and JNK. Treatment of cells with sphondin (50 microM) or the NF-kappaB inhibitor, PDTC (50 microM) partially inhibited IL-1beta-induced degradation of IkappaB-alpha in the cytosol and translocation of p65 NF-kappaB from the cytosol to the nucleus. Furthermore, IL-1beta-induced NF-kappaB-specific DNA-protein complex formation in the nucleus was partially inhibited by sphondin (50 microM) or PDTC (50 microM). Taken together, we demonstrate that sphondin inhibits IL-1beta-induced PGE(2) release in A549 cells; this inhibition is mediated by suppressing of COX-2 expression, rather than by inhibiting COX-2 enzyme activity. The inhibitory mechanism of sphondin on IL-1beta-induced COX-2 expression may be, at least in part, through suppression of NF-kappaB activity. We conclude that sphondin may have the therapeutic potential as an anti-inflammatory drug on airway inflammation. |
| References | 1. Acta Pol Pharm., 2003, 60(5), 391-393. 2. Life Sci., 2002, 72(2), 199-213. 3. SQU Journal For Science, 2004, 9, 7-17. |
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