In vivo treatment with the herbal phenylethanoid acteoside ameliorates intestinal inflammation in dextran sulphate sodium-induced colitis.
Recently we demonstrated that in inflammatory bowel disease (IBD) macrophage-oxidative burst activity is increased and NADPH oxidase mRNA is induced. The herbal phenylethanoid acteoside isolated from Plantago lanceolata L. was shown to exhibit anti-oxidative potential. Using the dextran sulphate sodium (DSS)-induced colitis model, in this study we have assessed whether systemic application of acteoside affects colitis. Colitis was induced by DSS in Balb/c mice. Treatment with acteoside (120, 600 microg/mouse/day) was performed intraperitoneally. The colon lengths were determined. Colonic tissue was scored histologically (max. score 8) by a blinded investigator. T cells isolated from mesenteric lymph nodes (MLN) were stimulated with anti-CD3 antibody in the presence of interleukin (IL)-2 (final concentration 10 U/ml). After incubation for 24 h, IL-1beta, IL-6, IL-12 tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma levels in supernatants were analysed by the beadlyte cytokine detection system. Histological scoring of colonic tissue revealed that application of acteoside was followed by a significantly improved histological score. In acute colitis the histological score was 3.2 with acteoside versus 5.2 with phosphate-buffered saline (PBS) (P < 0.02). In chronic colitis both 120 microg (3.3 versus 5.2) or 600 microg acteoside (3.0 versus 5.2) significantly ameliorated colitis (both P < 0.02). Stimulated MLN from mice with chronic DSS-induced colitis treated with acteoside showed a significant down-regulation of IFN-gamma secretion (195 pg/ml with 600 microg acteoside versus 612 pg/ml with PBS, P < 0.02). Inhibition of oxidative burst activity with acteoside reduced mucosal tissue damage in DSS colitis and could be a therapeutic alternative for IBD treatment. Further studies of this agent are warranted.
Hausmann
M
M
Department of Internal Medicine I, University of Regensburg, Germany. martin.hausmann@klinik.uni-regensburg.de
Obermeier
F
F
Paper
D H
DH
Balan
K
K
Dunger
N
N
Menzel
K
K
Falk
W
W
Schoelmerich
J
J
Herfarth
H
H
Rogler
G
G
D000208:Acute Disease; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002908:Chronic Disease; D003092:Colitis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D003106:Colon / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D005960:Glucosides / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009195:Peroxidase / Q000378:metabolism; D010636:Phenols / Q000627:therapeutic use*; D016897:Respiratory Burst / Q000187:drug effects; D015431:Weight Loss / Q000187:drug effects; D059808:Polyphenols
D000975:Antioxidants; D016207:Cytokines; D016264:Dextran Sulfate; D005960:Glucosides; D018836:Inflammation Mediators; D009195:Peroxidase; D010636:Phenols; C058956:acteoside; D059808:Polyphenols