title: Polysaccharide peptides from COV-1 strain of Coriolus versicolor induce hyperalgesia via inflammatory mediator release in the mouse.
abstract: Polysaccharide peptide (PSP), isolated from Coriolus versicolor COV-1, has been widely used as an adjunct to cancer chemotherapy and as an immuno-stimulator in China. In this study, the anti-nociceptive effects of PSP were investigated in two different pain models in the mouse. In the acetic acid-induced writhing model, initial studies showed that PSP decreased the number of acetic acid-induced writhing by 92.9%, which, by definition, would constitute an analgesic effect. However, further studies showed that PSP itself induced a dose-dependent writhing response. Studies on inflammatory mediator release showed that PSP increased the release of prostaglandin E2, tumor necrosis factor-alpha, interleukin-1beta, and histamine in mouse peritoneal macrophages and mast cells both in vitro and in vivo. The role of inflammatory mediator release in PSP-induced writhing was confirmed when diclofenac and dexamethasone decreased the number of writhing responses by 54% and 58.5%, respectively. Diphenhydramine totally inhibited the PSP-induced writhing. In the hot-plate test, PSP dose-dependently shortened the hind paw withdrawal latency, indicative of a hyperalgesic effect. The hyperalgesic effect was reduced by pretreatment with the anti-inflammatory drugs. In conclusion, the PSP-induced hyperalgesia was related to activation of peritoneal resident cells and an increase in the release of inflammatory mediators.
authors.affiliation: Department of Pharmacology, Faculty of Medicine, Basic Medical Sciences Building, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong SAR, China.
authors.forename: Siu-Lung
authors.initials: SL
authors.lastname: Chan
authors.forename: John H K
authors.initials: JH
authors.lastname: Yeung
mesh_terms: D000363:Agaricales / Q000737:chemistry*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D016207:Cytokines / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D006633:Histamine Antagonists / Q000494:pharmacology; D006636:Histamine Release / Q000187:drug effects; D006930:Hyperalgesia / Q000139:chemically induced* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D007375:Interleukin-1 / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D008813:Mice, Inbred ICR; D017288:Pain Threshold / Q000187:drug effects; D010455:Peptides / Q000494:pharmacology*; D011134:Polysaccharides / Q000494:pharmacology*; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D011930:Reaction Time / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D006633:Histamine Antagonists; D018836:Inflammation Mediators; D007375:Interleukin-1; D010455:Peptides; D011134:Polysaccharides; D011448:Prostaglandin Antagonists; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone