title: Protective effect of β-(1,3 → 1,6)-D-glucan against irritant-induced gastric lesions.
abstract: β-(1,3)-D-Glucan with β-(1,6) branches has been reported to have various pharmacological activities, such as anti-tumour and anti-infection activities, which result from its immunomodulating effects. Gastric lesions result from an imbalance between aggressive and defensive factors. In the present study, we examined the effect of β-(1,3)-D-glucan with β-(1,6) branches isolated from Aureobasidium pullulans on the gastric ulcerogenic response in mice. Oral administration of β-glucan ameliorated gastric lesions induced by ethanol (EtOH) or HCl. This administration of β-glucan also suppressed EtOH-induced inflammatory responses, such as infiltration of neutrophils and expression of pro-inflammatory cytokines, chemokines and cell adhesion molecules (CAM) at the gastric mucosa. Of the various defensive factors, the levels of heat shock protein (HSP) 70 and mucin but not PGE(2) were increased by the administration of β-glucan. β-Glucan-dependent induction of the expression of HSP70 and mucin proteins and suppression of the expression of pro-inflammatory cytokines, chemokines and CAM were also observed in cultured cells in vitro. The results of the present study suggest that β-glucan protects the gastric mucosa from the formation of irritant-induced lesions by increasing the levels of defensive factors, such as HSP70 and mucin.
authors: Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto, Japan.
authors: Ken-ichiro
authors: K
authors: Tanaka
authors: Yuta
authors: Y
authors: Tanaka
authors: Toshio
authors: T
authors: Suzuki
authors: Tohru
authors: T
authors: Mizushima
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D002277:Carcinoma / Q000188:drug therapy / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D005752:Gastric Mucins / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000648:ultrastructure; D005786:Gene Expression Regulation / Q000187:drug effects; D005936:Glucans / Q000627:therapeutic use*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007509:Irritants / Q000037:antagonists & inhibitors* / Q000633:toxicity; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020556:Neutrophil Infiltration / Q000187:drug effects; D020011:Protective Agents / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D013274:Stomach Neoplasms / Q000188:drug therapy / Q000378:metabolism; D013276:Stomach Ulcer / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D014407:Tumor Cells, Cultured
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015815:Cell Adhesion Molecules; D016207:Cytokines; D005752:Gastric Mucins; D005936:Glucans; D018840:HSP70 Heat-Shock Proteins; D018836:Inflammation Mediators; D007509:Irritants; D020011:Protective Agents; D012333:RNA, Messenger; C033671:epiglucan