2003 Fiscal Year Final Research Report Summary
The role of glial activation on the pathogenesis of septic encephalopathy
| Project/Area Number |
14571440
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Okayama University |
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Principal Investigator |
MATSUMI Masaki Okayama University, Hospitals, Assistant Professor, 医学部・歯学部附属病院, 講師 (70219476)
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| Co-Investigator(Kenkyū-buntansha) |
MIZOBUCHI Satoshi Okayama University, Hospitals, Assistant Professor, 医学部・歯学部附属病院, 講師 (70311800)
TAKAHASHI Toru Okayama University, Graduate School of Medicine and Dentistry, Research Instructor, 大学院・医歯学総合研究科, 助手 (40252952)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Sepsis / Heme Oxygenase / Carbon Monoxide / Endotoxin / Heme / Intestine / Oxidative stress / Inflammation |
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| Research Abstract |
Sepsis often leads to a multiple organ dysfunction syndrome (MODS), a leading cause of death in intensive care units. Symptoms of gram-negative bacterial sepsis can be reproduced experimentally by treatment of animals with LPS, a component of the cell wall of Gram-negative bacteria. LPS is responsible for initiating a series of highly complex cascading events leading to multiple organ damage. Reactive oxygen species are also thought to play an important role as an end-effector molecule. We examined the role of HO-1 induction in the intestinal tissue injury in a rat model of septic MODS produced by intraperitoneal injection of LPS. We found that HO-1 was markedly induced following LPS treatment in the mucosal epithelial cells in the Upper intestine such as the duodenum and the jejunum, whereas HO-1 was hardly expressed and not induced by the same treatment in the lower intestine such as the ileum and the colon. In contrast, the intestinal tissue injury acid inflammation was more pronounced in the lower intestine than in the upper intestine. Pretreatment of animals with HO-1 inhibitor augmented mucosal epithelial cell injuries and inflammation in the upper intestine, but not in the lower intestine, suggesting that HO-1 induction and the maintenance of its appropriate activity appear to be critical in the protection of the intestinal epithelial cells from an oxidative injury induced by LPS, or sepsis.
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Research Products
(4 results)
