2016 Fiscal Year Final Research Report
The gene therapy for sepsis by the clarification of STAT3 / SOCS3 which control an inflammatory or an anti-inflammatory reaction
| Project/Area Number |
25462809
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Emergency medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
GANDO SATOSHI 北海道大学, 大学院医学研究科, 教授 (30125306)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Keywords | 敗血症病態 / サイトカイン / IL-6 / TNF-αKO / 遺伝子治療 / Western Blotting / 敗血症脳症 / TNF-α |
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| Outline of Final Research Achievements |
LPS was administration to each thirty Wild type mice (WT-M) and IL-6 KO mice (IL-M).The case fatality was 96.7% and 46.7%. LPS was administration to each twenty-five Wild type mice (WT-M) and TNF-αKO mice (TNF-M). The case fatality was 100.0% and 32.0%.
The amplification efficiency of SOCS3 (SO-3) was a high price compared with STAT3 (ST-3). Moreover, in the LPS administration group, the amplification efficiency of SO-3 and ST-3 compared with the LPS non-administration group was together restrained. RT-PCR was performed using TNF-M. In TNF-M, the amplification efficiency of ST-3 was clearly restrained compared with SO-3 by the LPS administration group. Moreover, in the LPS non-administration group, the amplification efficiency of ST-3 was a high price in TNF-M compared with WT-M. It thought that the gene of the involvement of IL-6, TNF-α, i.e. 17q21.31 of ST-3 and 17q25.3 of SO-3 related to the developing of the septic clinical condition from above.
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| Free Research Field |
医歯薬学
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