Catalogue number | C100124 |
Chemical name | Catalposide |
CAS Number | 6736-85-2 |
Synonyms | Catalpin;(1aS,1bS,2S,5aR,6S,6aS)-1a,1b,2,5a,6,6a-hexahydro-6-[(4-hydroxybenzoyl)oxy]-1a-(hydroxymethyl)oxireno[4,5]cyclopenta[1,2-c]pyran-2-yl-b-D-Glucopyranoside |
Molecular Weight | C22H26O12 |
Formula | 482.4 |
Purity | 98% |
Physical Description | Powder |
Solvent | Chloroform, Dichloromethane,DMSO |
Storage | Stored at 2-8°C, Protected from air and light, refrigerate or freeze |
Applications | Catalposide is hypolipidemic by activation of PPARĪ± via a ligand-mediated mechanism that modulates the expression of in lipid metabolism genes in hepatocytes. Preliminary microarray-based gene expression test revealed that CATP, which alone did not significantly affect expression of any of the >8,000 genes analyzed, attenuated the expression of tumor necrosis factor-alpha (TNF-alpha)-induced proinflammatory genes including interleukin-8 (IL-8) in human intestinal epithelial HT-29 cells. Down-regulation of IL-8 mRNA accumulation was also reflected by the decreased IL-8 secretion in CATP-treated HT-29 cells. The signal transduction study revealed that CATP significantly attenuates TNF-alpha-mediated p38 and extracellular signal-regulated kinase (ERK) phosphorylation. Further, CATP reduced NF-kappaB-mediated transcriptional activation as well as Ikappa-Balpha degradation. To establish the in vivo relevance of these findings, we examined whether CATP could affect intestinal inflammation in vivo using the mouse model of trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. Intrarectal administration of CATP dramatically reduced the weight loss, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, CATP suppressed the expression of TNF-alpha, interleukin-1beta, and intercellular adhesion molecule-1 along with the inhibition of NF-kappa B p65 translocation into nucleus in TNBS colitis. Collectively, current results demonstrate that CATP may be an effective agent for the treatment of diseases characterized by mucosal inflammation. |
References | 1. Biochem Biophys Res Commun., 2012, 422(4), 568-572. 2. Inflamm Bowel Dis., 2004, 10(5), 564-572. 3. Archives of Pharmacal Research, 2009, 32(2), 207-213. 4. Analytical Letters, 2007, 36(14), 2999-3009. |
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