2017 Fiscal Year Final Research Report
The role of Nrf2 in organ and inflammatory cells during sepsis
| Project/Area Number |
16K20096
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology
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| Research Institution | Tottori University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | LPS / 敗血症 / Nrf2 / HO-1 / 酸化ストレス |
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| Outline of Final Research Achievements |
Sepsis is a syndrome triggered by endotoxin lipopolysaccharide (LPS) during bacterial infection. Vital organs may sometimes gain a tolerance against sepsis when exposed to an initial, LPS-induced sepsis, which prevents severe organ disorders on the occurrence of a second sepsis. Preconditioning (PC) is an endogenous protective mechanism by which sublethal damage confers tolerance to a subsequent lethal load. Oxidative stress is one of the important pathogenetic mechanisms that occur in sepsis. The nuclear factor erythroid 2 (NF-E2)-related factor-2 (Nrf2) system is a key regulatory transcription factor that protects organs and cells against oxidative stress and may be associated with the PC effect in repeated sepsis. Our results suggest that activation of the Nrf2 system is, at least in part, one of the mechanisms of a PC effect in the mouse liver in the case of repeated LPS stimulation.
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| Free Research Field |
麻酔科学
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