Kenta Nagai, MD
,
Departments of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan
Yoshitaka Ueno, PhD
,
Endoscopy, Hiroshima University, Hiroshima, Japan
Shinji Tanaka, PhD
,
Endoscopy, Hiroshima University, Hiroshima, Japan
Shintaro Sagami, MD
,
Hiroshima University Hospital, Hiroshima, Japan
Soki Nishiyama, MD
,
Departments of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan
Kei Shinagawa, PhD
,
Hiroshima University Hospital, Hiroshima, Japan
Shiro Oka, PhD
,
Endoscopy, Hiroshima University, Hiroshima, Japan
Toru Hiyama, PhD
,
Health Service Center, Hiroshima University, Higashihiroshima, Japan
Masanori Ito, PhD
,
Departments of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan
Yasuhiko Kitadai, PhD
,
Departments of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan
Masaharu Yoshihara, PhD
,
Health Service Center, Hiroshima University, Higashihiroshima, Japan
Kazuaki Chayama, PhD
,
Hiroshima University Hospital, Hiroshima, Japan
Ryohei Hayashi, MD
,
Departments of Gastroenterology and Metabolism, Hiroshima University, Hiroshima, Japan
Introduction: Non-steroidal anti-inflammatory drugs often cause ulcers in the human small intestine, but few effective agents exist to treat such injury. “
Ganoderma lucidum” Karst, also known as “Reishi”, is a mushroom. We previously reported that a water-soluble extract from
G.lucidumfungus mycelia (MAK) has anti-inflammatory effects in murine colitis. However, its effects on indomethacin-induced small intestinal injuries are unknown. The present study investigated the preventative effects of the polysaccharides derived from MAK on indomethacin-induced small intestinal injuries in mice.
Methods: Peritoneal macrophages (PMs) were stimulated in vitro with MAK, and adoptively transferred to C57BL/6 mice intraperitoneally, which were then given indomethacin. Intestinal inflammation was evaluated after 24 hours. We performed in vivo antibody blockade to investigate the preventive role of GM-CSF, which derived from PMs stimulated with MAK. We then used PMs stimulated with MAK pre-treated by pectinase in an adoptive transfer assay to investigate the preventive role of polysaccharides.
Results: Indomethacin-induced small intestinal injury was inhibited by adoptive transfer of PMs stimulated in vitro with MAK. In this transfer model, pre-treatment with anti-GM-CSF antibody reversed the improvement of small intestinal inflammation by indomethacin. PMs stimulated with pectinase-pretreated MAK impaired the anti-inflammatory effect of MAK.
Conclusion: PMs stimulated by MAK appear to contribute to the anti-inflammatory response through GM-CSF in small intestinal injury induced by indomethacin. The polysaccharides from G.lucidum may elicit anti-inflammatory effect.
