lancemaside-a and Colitis

lancemaside-a has been researched along with Colitis* in 2 studies

Other Studies

2 other study(ies) available for lancemaside-a and Colitis

ArticleYear
Echinocystic acid, a metabolite of lancemaside A, inhibits TNBS-induced colitis in mice.
    International immunopharmacology, 2013, Volume: 15, Issue:2

    The rhizome of Codonopsis lanceolata (CL, family Campanulaceae), of which the main constituent is lancemaside A, has been used for cough and bronchitis in traditional Chinese medicine. To evaluate anti-colitic effect of CL, we examined anti-inflammatory effect of CL extracts, lancemaside A and its metabolites in lipopolysaccharide (LPS)-stimulated peritoneal macrophages and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. Among CL extracts, CL BuOH extract inhibited LPS-induced IL-1β, IL-6 and TNF-α expression, as well as NF-κB activation most potently. CL BuOH extract also inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice. Among lancemaside A, a main constituent of CL BuOH extract, and its metabolites (lancemaside X, echinocystic acid-3-O-β-d-glucopyranoside and echinocystic acid), echinocystic acid inhibited the expression of the pro-inflammatory cytokines, IL-1β, IL-6, and TNF-α, as well as the phosphorylation of IKKβ and p65 in LPS-stimulated peritoneal macrophages most potently. Echinocystic acid also potently inhibited the binding of LPS to TLR4 on peritoneal macrophages. Lancemaside A and its metabolite, echinocystic acid, inhibited TNBS-induced colonic inflammation, including colon shortening, increased myeloperoxidase activity and pro-inflammatory cytokine expression, and NF-κB activation in mice. The anti-colitic effect of echinocystic acid was superior to that of lancemaside A. Based on these findings, orally administered lancemaside A may be metabolized to echinocystic acid, which may express anti-colitic effect by inhibiting the binding of LPS to TLR4 on the macrophages.

    Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Cells, Cultured; Codonopsis; Colitis; Colon; Cytokines; Humans; Inflammation Mediators; Lipopolysaccharides; Macrophages, Peritoneal; Male; Medicine, Chinese Traditional; Mice; Mice, Inbred ICR; NF-kappa B; Oleanolic Acid; Protein Binding; Rhizome; Saponins; Signal Transduction; Toll-Like Receptor 4; Trinitrobenzenesulfonic Acid

2013
Lancemaside A ameliorates colitis by inhibiting NF-kappaB activation in TNBS-induced colitis mice.
    International journal of colorectal disease, 2010, Volume: 25, Issue:5

    In a preliminary study, we found that lancemaside A, which is a main constituent of Codonopsis lanceolata used as an herbal medicine for inflammatory diseases, potently inhibits lipopolysaccharide (LPS)-stimulated, TLR-4-linked NF-kappaB activation of NF-kappaB luciferase reporter gene-transfected 293-hTLR4-hemagglutinin (HA) cells. Therefore, we investigated its inhibitory effect in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice.. We measured the ability of lancemaside A to inhibit LPS-stimulated, TLR-4-linked NF-kappaB activation in human embryonic kidney (HEK) cells, as well as to inhibit colitis outcomes in TNBS-induced colitis in mice. We also measured levels of the inflammatory markers, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and IL-6, and their transcription factor, NF-kappaB, in intestinal mucosa by enzyme-linked immunosorbent assay and immunoblotting.. Intrarectal treatment of TNBS in mice caused colon shortening and also increased colonic expression of IL-1beta, IL-6, and TNF-alpha expression. Oral administration of lancemaside A (10 and 20 mg/kg), inhibited colon shortening and myeloperoxidase activity in TNBS-induced colitic mice and also decreased colonic expression of IL-1beta, IL-6, and TNF-alpha. Lancemaside A inhibited NF-kappaB activation induced by TNBS, as well as the expression of cyclooxygenase 2 and TLR-4. Lancemaside A also reduced the activity of intestinal bacterial beta-glucuronidase that was induced by TNBS.. Lancemaside A ameliorates colitis via inhibition of TLR-4-linked NF-kappaB activation.

    Topics: Animals; Cell Line; Colitis; Cyclooxygenase 2; Cytokines; Feces; Glucuronidase; Humans; Hyaluronic Acid; Inflammation Mediators; Lipopolysaccharides; Mice; NF-kappa B; Saponins; Toll-Like Receptor 4; Trinitrobenzenesulfonic Acid

2010